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Cadmium (Cd) is a heavy metal to which humans are exposed both occupationally and environmentally. For many years cadmium has been understood as a toxic element to human health, and an elevated level of cadmium exposure has been shown to be related to adverse reproductive effects, especially in men. In this review we studied published data about the toxic effects of this trace element on the total male reproductive system, including gonadal development, testes, testosterone, spermatogenesis and accessory sex glands, to clarify how cadmium causes male fertility problems. For this purpose, in the next sections after introducing this trace element thoroughly, we will separately mention cadmium's effects on each part of male reproductive system.
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Journal of Infertility and Reproductive Biology, 2014, Volume 2, Issue 2, Pages: 62-69
Cadmium and male infertility
Alaee S
, Talaiekhozani A
, Rezaei S
, Alaee K
, Yousefian E
1. Department of Reproductive Biology, School of Advanced Medical Sciences and Technologies, Shiraz
University of Medical Sciences, Shiraz, Iran
2. Institute of Environmental and Water Resources Management, Water Research Alliance, Universiti
Teknologi Malaysia, UTM Skudai, 81310 Johor Bahru, Malaysia
3. Jami Institute of Technology, Department of Civil Engineering, Isfahan, Iran
4. Department of Obstetrics and Gynecology, Shiraz University of Medical Sciences, Shiraz, Iran
5. Department of Radiology, Shiraz University of Medical Sciences, Shiraz, Iran
6. Department of Midwifery, Falavarjan Branch, Islamic Azad University, Isfahan, Iran
Cadmium (Cd) is a heavy metal to which humans are exposed both occupationally and environmentally. For
many years cadmium has been understood as a toxic element to human health, and an elevated level of cadmium
exposure has been shown to be related to adverse reproductive effects, especially in men. In this review we studied
published data about the toxic effects of this trace element on the total male reproductive system, including gonadal
development, testes, testosterone, spermatogenesis and accessory sex glands, to clarify how cadmium causes male
fertility problems. For this purpose, in the next sections after introducing this trace element thoroughly, we will
separately mention cadmium’s effects on each part of male reproductive system.
Keywords: Cadmium, Male, Testis, Sperm, Reproduction
1. Introduction
Heavy metals are natural components of the
earth’s crust and cannot be degraded or destroyed.
Cadmium is a heavy metal, used in industrial
activities such as the manufacture of nickel-cadmium
batteries, electroplating, pigments, ceramics, plastic
stabilizers, and fertilizers, as well as in other
industrial, mining, agricultural activities and in the
widespread use of phosphate-based fertilizers (1-3).
Consequently, there is a high level of cadmium
contamination at many locations worldwide, which
leads to pollution of the water and air. After cadmium
enters the environment, it pollutes air and water and
at last is discharged into the food chain, detrimentally
affecting living organisms (4, 5). The toxicity of
cadmium was first described by Friedrich Stromeyer
in 1817. In the 1940s, environmental exposure to
Corresponding Address: Dr. Sanaz Alaee, School
of Advanced Medical Sciences and Technologies,
Shiraz University of Medical Sciences, Shiraz, Iran.
cadmium’s toxicity was reported in Japan’s Jinzū
river basin, where a disease called itai-itai tormented
many people. These patients showed a wide range of
symptoms, such as low-grade bone mineralization, a
high rate of fracture, an increased rate of osteoporosis
and intense bone-associated pain. This affliction
occurred because the river basin’s inhabitants had
consumed local rice, which had been grown in fields
irrigated with cadmium-contaminated water (3).
Cadmium has molecular homology with zinc and
calcium and compensates with them for resorption to
the body (6, 7). Studies have shown that in humans,
cadmium can be absorbed into the body through the
gastrointestinal, respiratory and dermal systems (8).
The major source of inhalative cadmium intoxication
is smoking, and the human lung resorbes 40-60% of
the cadmium content in cigarette smoke (9). As a
result, smokers receive a dose of cadmium daily and
generally have cadmium blood levels 4-5 times more
than those of nonsmokers (2, 8, 10). In nonsmokers,
most uptake of cadmium is through cadmium-
Journal of Infertility and Reproductive Biology, 2014, Volume 2, Issue 2, Pages: 62-69
contaminated drinking water and food, particularly
cereals, such as rice and wheat, and also potato and
green leafy vegetables (2, 8, 10, 11).
It has been documented that the total amount of
cadmium uptake to the human body depends on the
consumed dose. Several factors can increase this
uptake, such as low intake of vitamin D, calcium and
iron (8). It has been demonstrated that cadmium
uptake in people with anemia and habitual iron
deficit, such as children or menstruating women, is
higher than in other people (12). In addition, it is
estimated that dietary intake of cadmium is higher in
men than women (13).
A higher level of cadmium intake, more than the
standard level, has an significant adverse effect on
growth rate (14, 15), but its toxic effects on tissues
are not the same in all tissues, i.e., vary from tissue to
tissue and are seen primarily in sensitive tissues such
as liver, kidney, ovary and especially testes (16).
Studies of cadmium toxicity have introduced it as
an ubiquitous environmental human carcinogen (17)
and one of the best-known reproductive toxicants in a
wide variety of animals (18-22). In humans, chronic
exposure to environmentally-relevant cadmium
results in high cadmium level, especially in infertile
men (23, 24). Therefore, in the current study we
reviewed available literature to determine which part
of the male reproductive system is most affected by
cadmium and how cadmium causes male fertility
2. Effects of cadmium on gonadal development
Collected data showed that cadmium affects the
male reproductive system from embryonic stages to
adulthood, and has adverse effects on gonadal
development (25). In mouse embryos, administration
of cadmium caused reduced genital ridge size and
retarded migration of germ cells into the genital
ridges, resulting in attenuated populations of germ
cells, aberrant maturation of gametes and subfertility
(26). In young rabbits treated with 1.0-2.25 mg/kg
body weight cadmium, significant damage to the
germinal epithelial and basement membrane after 48
hours and a significant reduction in the volume of
epididymis epithelium after 5 months’ treatments
were observed (27).
3. Effects of cadmium on reproductive system
3.1. Testes
Testis is one of the tissues that is very sensitive to
the toxic effects of cadmium. Elevated accumulation
of cadmium in testis has been measured using atomic
absorption spectroscopy technique and confirmed by
the presence of hyperchromatic cadmium precipitants
in histological sections of seminiferous tubules of
adult male mice treated with cadmium (15).
Similarly, gonadal damage has been shown to
develop following administration of cadmium to
adult male rats either orally or subcutaneously (25).
In humans, testicular cadmium levels are age
dependent and elevate after the fourth decade of life
(28). Some studies show that cadmium accumulation
in the testes has no effect on testicular weight (29-
31), but there is some evidence showing that the
weight of testis can be affected by cadmium
accumulation in testicular tissue, rather than by total
body weight; however, this depends on the level of
applied cadmium, duration of treatment and the level
of cadmium concentration in the testis (Table 1) (14,
15, 32, 33). Additionally, cigarette smoking has been
reported to be associated with decreased testis size in
men, related to the cadmium content of cigarettes
Cadmium enters the seminiferous tubules through
a breach of the blood-testis barrier and causes focal
testicular necrosis and dystrophy with consequent
reduction in germ cell numbers, leading to infertility
(15, 25, 35, 36). Disruption of the blood-testis barrier
by cadmium is a consequence of endothelial cell
damage in testicular blood vessels and separation of
endothelial cells, which has been confirmed by light
and electron microscopy and is mediated by reduced
occludin protein expression, indicating the involve-
ment of cell junction breakdown in blood-testis
barrier disruption (35-37).
Researchers report that high concentration of
reactive oxygen species (ROS), generated by
accumulation of cadmium in testicular tissue, exceeds
the antioxidant capability of the testis cells, leading to
lipid peroxidation, degeneration of seminiferous
tubules, testicular hemorrhage, testicular necrosis,
abnormal Leydig cells, fibrosis and reduced testicular
size. Therefore, severe cellular injury in seminiferous
tubules could be due to a high level of peroxidation
in lipid membrane of testicular cells, observed in
many studies (14, 15, 25, 33, 38-45). In one study by
Monsefi et al., (2010) administration of cadmium
chloride caused severe damage to seminiferous
tubules, resulting in difficulty in identification of
seminiferous tubules by light microscope and also
consequent reduction in spermatogenesis, as there
was no spermatozoid in the lumen of some
seminiferous tubules (15).
3.2. Testosterone
Testosterone is the principle male sex hormone
produced by Leydig cells, located in interstitial tissue
of testis. Presence and function of this hormone is
Journal of Infertility and Reproductive Biology, 2014, Volume 2, Issue 2, Pages: 62-69
crucial for accurate spermatogenesis process of
seminiferous tubules, and evaluation of the plasma
testosterone level is considered a useful indicator of
testicular function (46, 47).
While many studies have been suggested that
cadmium increases testosterone level (29, 48, 49),
others showed that cadmium administration
attenuates it (14, 15, 21, 50-54). However, according
to Table 1, it can be concluded that the effect of
cadmium on testosterone level is dependent on dose,
duration and method of cadmium administration. In
addition, modified Leydig cells in the interstitial
tissue of testes of mice exposed to cadmium chloride
have been reported (15). Nevertheless, we should
mention that except for serum, the evaluation of testi-
cular testosterone is important, and testicular
testosterone levels are approximately one hundred
fold higher than serum testosterone levels, and this
high level is required to support spermatogenesis (55,
Consequently, it is possible that testicular
testosterone level can be more sensitive to the effects
of cadmium than serum level, as was observed in rats
treated with cadmium (14). Telisman et al. (2000)
showed that cadmium has the ability to impair male
fertility without effects on the male reproductive
endocrine function (57). So it is concluded that
cadmium affects testosterone synthesis through
various mechanisms that depend upon experimental
Table 1. Studies about effects of cadmium on weight of testes, accumulation of cadmium in testes and plasma
testosterone level.
Model of
Doses of
Weight of
of cadmium in
level Reference
Adult Wistar
male rats Subchronic
exposure to Cd (CdCl2, 40 mg/l,
per os) 30 days S Decrease NE S Decrease in
plasma and
testis (14)
BALB/c male
by gavage
23 mg/kg
BW 45 days NS Decrease NS Increase S Decrease (15)
50 mg/kg
BW once per day S Decrease S Increase S Decrease
Adult Wistar
male rats Orally CdCl
mg/kg) 15 days NE S Increase S Decrease (21)
Adult Wistar
male rats
radish bulb
1.1 µg Cd/g of
4 weeks No change S Increase NS Increase
8 weeks No change S Increase S Increase
12 weeks No change S Increase NS Decrease
Dawley male
Subcutaneously 0.6 mg Cd/kg
once per day 6 weeks No Change S Increase NE (31)
Dawley male
by gavage
, 5 mg/kg
BW 15 days S Decrease NE NE (33)
Adult Swiss
Webster male
injection once a
0.1 mg/kg
BW once per
4, 10, 26,
and 52
weeks NE S Increase NS Increase (48)
S= Significant; NS= Non significant; NE= Not examined.
3.3. Spermatogenesis and semen parameters
Besides being detected in blood, cadmium can be
identified in seminal plasma of cigarette smokers
(58), but no relationship was reported between the
levels of cadmium in blood and seminal plasma (59,
In the literature, conflicting evidence exists
regarding the correlation between the cadmium
content of seminal plasma and semen parameters (20,
60-63). Where some studies demonstrated positive
correlation between the cadmium content of semen
and seminal quality (60, 64), others reported that
seminal plasma cadmium level is unrelated to semen
parameters and also fertility status (64-66).
Studies suggest that different cell populations within
the testis can be as targets of cadmium toxicity (67,
68), and cadmium is able to be accumulated in
germinal cells such as spermatogonia, spermatocytes,
Journal of Infertility and Reproductive Biology, 2014, Volume 2, Issue 2, Pages: 62-69
spermatid and spermatozoa after the entrance of
cadmium to testicular tissue (31, 44, 48). In one
study, Sprague Dawley rats subcutaneously injected
with daily 0.6 mg/kg doses of cadmium over a 6-
week period developed an accumulation of cadmium
in the testes, mainly in spermatogonia and
spermatocytes, with consequent reduction in both of
these cell types (31). However, in one study which
used atomic absorption spectroscopy and particle-
induced x-ray emission analyses, the presence of
cadmium in germinal cells was not observed (48).
As shown in Table 2, treatment with different
doses and durations of cadmium leads to sperm
concentration reduction (14, 15, 21, 29, 31, 33).
Haouem et al. (2008) observed that by increasing the
duration of cadmium administration, sperm
concentration decreases in male rats mainly because
of high apoptosis of sperm cells (29), which was seen
in male cigarette smokers, too, especially in heavy
smokers. Therefore, cadmium could be a possible
causative agent for the low sperm density among
smokers (69).
Besides sperm concentration, sperm motility is
also severely affected by cadmium. Sperm motility is
recognized to be more sensitive to this trace element,
as reduced sperm motility has been observed at a
dose far below the dose affecting sperm production.
However, it is concluded that cadmium accumulation
in germinal cells and cadmium effects on sperm
count and sperm motility are dose- and time-
dependent (Table 2) (14, 24, 25, 27, 31, 70). Taha et
al. (2012) observed that men with idiopathic male
infertility had higher seminal cadmium levels (71),
which was correlated with impairment of sperm
motility, especially progressive sperm motility, lower
percentages of viable sperms and more important,
with higher sperm DNA fragmentation and semen
ROS level (71).
Regarding the adverse effects of this heavy metal
on sperm motility, some studies have suggested that
motility of sperm can be used as an early and
sensitive endpoint for the assessment of cadmium
toxicity in the male reproductive system (59).
Table 2. Effects of cadmium on semen parameters.
Model of
method Doses of cadmium Duration
treatment Sperm count Sperm motility Reference
Adult Wistar
male rats
Subchronic exposure
to CdCl
40 mg/l, per os 30 days S Decrease S Decrease (14)
Adult BALB/c
male mice Orally administration
of CdCl
23 mg/kg BW, once per
day 45 days NS Decrease NS Decrease (15)
50 mg/kg WB, once per
45 days S Decrease S Decrease
Adult Wistar
male rats Oral administration of
mg/kg) 15 days S Decrease NE (21)
Adult Wistar
male rats Cd-contaminated
radish bulb 1.1 µg Cd/g of diet
4 weeks NS Decrease NE
8 weeks NS Decrease NE
12 weeks S Decrease NE
Adult Sprague
Dawley male
injection 0.6 mg Cd/kg once per day 6 weeks S Decrease in
testicular SG
and SC NE (31)
Adult Sprague
Dawley male
Oral administration of
5 mg/kg BW 15 days S Decrease S Decrease (33)
Adult male rats CdCl
1 mg kg 3 days S Decrease S Decrease (45)
S= Significant; NS= Non significant; NE= Not examined; SG= Spermatogonia; SC= Spermatocyte.
3.4 Sperm chromatin integrity and DNA stability
hromatin condensation and DNA stability are
indices of sperm quality, which can be identified
through aniline blue and acridine orange,
respectively, to reflect the possible disorders in sperm
DNA and sperm maturation. Damage to sperm DNA
seems to affect embryo and increases the risk of
infertility, miscarriage, or serious diseases in the
offspring (72, 73). Through the use of acidic aniline
blue staining, it has been revealed that cadmium can
inhibit the chromatin condensation process, which is
important for sperm maturation. This is a significant
Journal of Infertility and Reproductive Biology, 2014, Volume 2, Issue 2, Pages: 62-69
limiting factor in fertility potential; but incorporation
of cadmium into sperm chromatin was not confirmed
using Acridine orange staining (15).
3.5. Prostate and Seminal Vesicle
Although some studies have suggested the
carcinogenic potential of cadmium on prostate tissue
(17, 74), a critical study by Sahmoun et al. (2005) has
shown that in contrast to laboratory animals,
epidemiological analyses do not convincingly
implicate cadmium as a cause of prostate cancer (75).
Exposure of rats to Cd resulted in a significant
reduction in seminal vesicle (14, 15). Monsefi et al.
(2010) showed that administration of cadmium to
male mice causes reduced weight of seminal vesicles
and high serum prostatic acid phosphatase activity.
These effects may be due to hypertrophy or
hyperplasia of the prostate gland, leading to increased
synthesis or expression of this enzyme (15).
4. Conclusion
According to the literature, cadmium has adverse
effects on the male reproductive system and the testes
are the main target of cadmium.
Cadmium enters the body through contaminated
air, water and food. It then circulates in the blood and
reaches tissues such as testis, where it accumulates.
Cadmium in the testis disrupts the blood-testis
barrier, comes into close contact with different cells
of testis and, by increasing the production of ROS
and decreasing various antioxidants’ levels, enhances
the lipid peroxidation of cell membranes, causes
apoptosis and necrosis of all testicular tissue leading
to disturbance of spermatogenesis, reduces sperm’s
motility and finally leads to infertility.
Also oxidative damage of sperm’s DNA causes
paternal genomic disorder contributed to a variety of
developmental disorders including early or late
embryonic lethality. However, with regard to the
literature, studies have failed to demonstrate the
incorporation of cadmium into sperm chromatin.
In conclusion, subfertility following cadmium
administration might result from penetration of
cadmium to testicular tissue and damage to testicular
tissue, leading to disturbance of the testes’ function,
manifested by disruption of spermatogenesis and
sperm motility, with or without effects on the male
reproductive endocrine function.
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... The plant is reported to contain steroidal saponins, flavonoids and homoisoflavonoids (Ding et al., 1989;Botura, 2010), Studies (Santos et al., 2009, Cerquerira et al., 2012) have documented the different pharmacological properties of A. sisalana, but its effects on semen parameters have not been documented. According to Alaee et al., (2014), Cadmium (Cd) has adverse effects on the male reproductive system and the testes are the main target of cadmium. Cadmium enters the body through contaminated air, water and food. ...
... It then circulates in the blood and reaches tissues such as testis, where it accumulates. Cadmium disrupts the blood-testis barrier, comes into close contact with different cells of testis and, by increasing the production of ROS and decreasing various antioxidants' levels, enhances the lipid peroxidation of cell membranes, causes apoptosis and necrosis of all testicular tissue leading to disturbance of spermatogenesis, reduces sperm's motility and finally leads to infertility (Alaee et al.,2014). Tam and Liu (1985) reported that in rats, cadmium caused diminished sperm count and impeded movement of sperm cells, resulting in a weakened typical case of infertility. ...
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The effect of aqueous root extract of Agave sisalana Perr. Synon on the semen parameters and serum testosterone level of cadmium-intoxicated male Wistar rats was investigated. Twenty five male rats were divided into five groups of five animals each (Groups I-V). Cadmium (0.2 mg/kg) was administered for seven days to induce reproductive toxicity. The animals were grouped and treated thus; Group 1 (normal control without cadmium), Group II (Cadmium control group) while Groups III-V were dosed orally with 50, 100 and 150 mg/kg of the aqueous root extract of A. sisalana for fourteen days after cadmium intoxication. The serum testosterone level and semen parameters were determined. There was a significant difference in the serum testosterone level between treated rats and control. The sperm count, sperm motility and sperm morphology were significantly (p < 0.05) increased in the extract-treated rats compared with the Cadmium control group. The result suggested that the A. sisalana root extract has the potential to improve male reproductive function and promote fertility which might be a consequence of both its potent antioxidant properties and androgenic activities.
... Cadmium (Cd) is a widespread environmental pollutant that is considered as one of the most toxic heavy metals. Due to its unique physico-chemical properties [1], cadmium has several industrial uses, such as paints and electrolysis industry [2], fertilizers and battery manufacturing [3]. Cd can be found in certain drinks, meat, grains as well as in cigarette. ...
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The purpose of the present study was to assess the protective effects of ‘Opuntia ficus indica’ (family Cactaceae) against osteoporosis induced by cadmium chloride in female Wistar rats. Experiments were carried out on 36 male Wistar rats (6-8 weeks old) divided into four groups of nine each: a control group, a group treated with cadmium (3,5 mg/kg /day) by subcutaneous injection, a group treated with Opuntia ficus indica extract (100 mg/Kg/day) by gavage, and a group treated with opuntia extract then treated with cadmium. After 10 weeks of treatment, animals from each group were rapidly sacri?ced by decapitation. Blood serum was obtained by centrifugation. Bone toxicity was estimated by examining femoral length and weight, calcium, phosphorus, vitamin D3 and alkaline phsphatase (ALP) levels, oxidative status and DNA aspects in femur tissue. Results showed that cadmium could induce hypocalcemia, hypophosphatemia, Vit D deficiency, increase in ALP level, and decrease in femur weight and length. Also, an oxidative stress evidenced by statistically signi?cant losses in the activities of catalase (CAT), superoxide-dismutase (SOD), glutathione-peroxidase (GPX) activities and an increase in lipids peroxidation level in bone tissue of cadmium-treated group compared with the control group. In addition, histological analysis in bone tissue of cadmium-induced rats revealed pronounced morphological alterations with areas of bone resorption and a loss of normal architecture of femur diaphysis bone as well as DNA fragmentation. However, administration of cactus extract attenuated cadmium-induced bone damage. The protective effect of the plant can be attributed to its antioxidant properties and the existence of phenolic acids and flavonoids, as highlighted by HPLC-based analysis. These findings indicate that ‘Opuntia ficus indica’ extract, can be used as a new option in nutraceutical field.
... The testis has been identified asj a significant site of Cd toxicity as it is extremely vulnerable to the effects of low Cd levels that would have no deleterious consequences in other tissues (Alaee et al., 2014;Alirezaei et al., 2012;Kumar et al., 2016;Rania & Mohamed, 2014). The exact pathophysiology of Cd developmental and sexual impairment has not been elucidated, but oxidative stress has been associated with Cd toxicity in several studies Ognjanovi et al., 2010). ...
In the current study, we synthesized and prepared a curcumin and vitamin E nanocomposite coated with olive oil (CEONC). Curcumin, vitamin E, and olive oil are fundamental organic antioxidants, and forming nanoparticles from these components endows them with special characteristics. We investigated the protective effect of CEONC on reproductive toxicity induced by cadmium chloride (CdCl2) in male rats. Forty rats (170–180 g) were randomly assigned to four groups: Group 1 (control) received oral distilled water; Group 2 intraperitoneal injection with CEONC (30 mg/kg); Group 3 received oral CdCl2 (5 mg/kg); and Group 4 received CdCl2 (5 mg/kg) followed by CEONC (30 mg/kg) for 4 weeks. After 50 days, we terminated the experiment and assessed male reproductive hormones, sperm motility, viability and morphology, and testes histopathology and conducted a comet assay. The results revealed that co-administration of CEONC with CdCl2 exposure increased reproductive hormone levels, improved sperm motility and viability, prevented sperm morphological changes, recovered the testicular histology, and decreased DNA damage in the testicular tissue compared to rats exposed to CdCl2 alone. CEONC administration produced no adverse effects and enhanced all sperm parameters. Our findings demonstrate that CEONC is a potential treatment for preventing reproductive damage induced by cadmium exposure.
... Testosterone is important in the development and functioning of androgendependent reproductive organs such as the prostate, seminal vesicles and epididymis (Dohle et al. 2015). Cd causes cellular degeneration in the prostate and reduces the weight of the seminal vesicles in rats and mice and the epididymis in rabbits (Alaee et al. 2014). ...
Cadmium (Cd) is a heavy metal related to a decrease in sperm parameters. The transit of spermatozoa through the epididymis is necessary to generate changes in the sperm membrane, such as the assembly of various carbohydrates that are added to the spermatazoan's surface to prepare it for successful fertilisation of the oocyte. No studies have yet analysed whether Cd alters the presence and distribution of these carbohydrates. We aimed to evaluate the changes induced by Cd in the distribution pattern of N-acetylglucosamine, sialic acid, mannose and fucose on the sperm membrane in the epididymis (e.g. caput, corpus, cauda) and if it alters the epididymal epithelium. Male Wistar pups were treated with Cd doses (0.125, 0.25 and 0.5mg/kg) on postnatal days 1-49. At postnatal day 90, they were humanely killed, sperm samples were obtained from the epididymis and tissue samples were taken for histological analysis. Cd concentrations in the blood and epididymis increased in proportion to the dose administered and decreased the serum testosterone levels and sperm quality. Histological analysis revealed alterations in the epithelium in all Cd-treated groups. Cd altered the distribution patterns of carbohydrates and fluorescence indices. All these alterations affected the structure and functioning of sperm.
... Testosterone plasma level is a useful indicator of testicular function. 1 Inside Sertoli cells, testosterone is bound to androgen receptors. Activation of these receptors results in initiation and maintenance of spermatogenesis and prevents germ cells apoptosis. ...
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Introduction: Hypercholesterolaemia affects Sertoli and Leydig cells secretory functions, impairs steroid hormones biosynthesis, and disrupts the hypothalamic-pituitary-gonadal axis. The use of honey in previous studies resulted in an improvement of male reproductive hormonal disturbances. This study aimed to investigate the protective effects of Trihoney on hypercholesterolaemia-induced male reproductive hormonal changes in male rabbits and compare its effects with atorvastatin. Materials and methods: Forty-eight male New Zealand white rabbits were assigned into 6 groups as follows; Control: commercial pellet; CH: commercial pellet with 0.6 g/kg/day Trihoney; HCD: 1% cholesterol diet; DH1: 1% cholesterol diet with 0.3 g/kg/day Trihoney; DH2: 1% cholesterol diet with 0.6 g/kg/day Trihoney and DAt: 1% cholesterol diet with 2mg/kg/day atorvastatin. After 12 weeks, the rabbits were sacrificed and blood samples were collected for analysis of hormones and pro-inflammatory cytokines and calculation of HOMA-IR. The testes were homogenized for intra-testicular testosterone measurement. Results: Serum testosterone reduced significantly in HCD (p<0.05) and DAt (p<0.05) groups. Likewise, intra-testicular testosterone reduced significantly in HCD (p<0.01) and DAt (p<0.01) groups. Serum FSH increased significantly in HCD (p<0.001) and DAt (p<0.01). Trihoney particularly at the dose of 0.6 g/kg/day improved serum and intra-testicular testosterone (p<0.05) and FSH (p<0.05). Trihoney and atorvastatin improved serum pro-inflammatory cytokines. Trihoney and atorvastatin did not affect HOMA-IR. Conclusion: Trihoney attenuated the detrimental effects of hypercholesterolaemia on male reproductive hormones which probably through a local effect on testicular tissue and Trihoney anti-inflammatory effect independent of insulin resistance. Atorvastatin did not counteract the impact of hypercholesterolaemia on the reproductive hormones.
Cadmium (Cd) is ubiquitous in our environment and can easily bioaccumulate into the organism after passage through the respiratory and digestive tracts. Long-term exposure to Cd can result in the significant bioaccumulation in organism because of its long biological high-life (10–30 years), which exerts irreversible damages on the health of animals and humans. Although there are increased evidence of impeding the normal function of female reproduction resulted from Cd exposure, the mechanism of the negative action of Cd on the growth and development of ovarian follicle remains enigmatic. Thus, the purpose of the presented study is to summarize available literature which describing Cd-related toxicity involved in the adverse effects on the growth and development of the ovarian follicle. In conclusion, it is suggested that Cd causes damage to the folliculogenesis of mammalians, which results in the decline in the number and quality of ovulated oocytes and the failure in the fertilization. The mechanism behinds that may be linked to the interference to the production of reproductive hormones and the augment of reactive oxygen species (ROS). Furthermore, the enhanced ROS, in turn, impairs various molecules including proteins, lipids and DNA, as well as the balance of the antioxidant defense system, mitochondrial homeostasis, endoplasmic reticulum, autophagy and epigenetic modification. This review is expected to elaborate the toxic mechanism of Cd exposure to the growth and development of ovarian follicles and provide essential remediation strategies to alleviate the damage of Cd to female reproductive health.
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Hypogonadism is an endocrine disorder characterized by inadequate serum testosterone production by the Leydig cells of the testis. It is triggered by alterations in the hypothalamic–pituitary–gonadal axis. Erectile dysfunction (ED) is another common disorder in men that involves an alteration in erectile response–organic, relational, or psychological. The incidence of hypogonadism and ED is common in men aged over 40 years. Hypogonadism (including late-onset hypogonadism) and ED may be linked to several environmental factors-induced oxidative stresses. The factors mainly include exposure to pesticides, radiation, air pollution, heavy metals and other endocrine-disrupting chemicals. These environmental risk factors may induce oxidative stress and lead to hormonal dysfunctions. To better understand the subject, the study used many keywords, including “hypogonadism”, “late-onset hypogonadism”, “testosterone”, “erectile dysfunction”, “reactive oxygen species”, “oxidative stress”, and “environmental pollution” in major online databases, such as SCOPUS and PUBMED to extract relevant scientific information. Based on these parameters, this review summarizes a comprehensive insight into the important environmental issues that may have a direct or indirect association with hypogonadism and ED in men. The study concludes that environmental factors-induced oxidative stress may cause infertility in men. The hypothesis and outcomes were reviewed critically, and the mechanistic approaches are applied through oxidant-sensitive pathways. This study also provides reccomendations on future therapeutic interventions and protective measures against such adverse environmental factors-induced hypogonadism and ED.
Among the xenobiotics of diverse nature, heavy metals are especially dangerous for the human reproductive system in case of excessive intake. Cadmium, which is one of the most common toxic substances for the environment and production, can pose a potential threat to human health. An increasing amount of cadmium in the environmental objects and in nutrition is believed to be related to a poor semen quality. The purpose of the study was to determine the impact of cadmium on the reproductive potential of men who live in ecologically contrasting conditions. Material and methods. Clinical and hygienic assessment of the reproductive health was carried out among 2 experimental groups: the 1st group consisted of fertile men living in the city of Dnipro (62 respondents), the 2nd group included men with normal fertility living in the control city (37 respondents). To determine the cadmium concentration, venous blood samples and ejaculate were selected according to the standard methods. Biological samples were transferred to aliquots, frozen and stored at -20 ° C until analysis. The research was carried out using inversion voltammetry on the device AVA-2. Statistical processing of the results was carried out using statistical software packages of statistical analysis Statistica v.6.1 (StatsoftInc., США, licence NAJAR909E415822FA), Microsoft Excel. Results and discussion. Cadmium content in the blood and in the sperm of the fertile men of industrial city 1.3-5.8 times higher than the results of research in the control city and literature data. Differences between the cadmium content in the blood and semen of fertile men was shown to be unlikely, suggesting that the hematotesticular barrier is insufficient to protect the male reproductive organs from the toxic effects of the metal. The ejaculate in the fertile men of the studied cities is characterized by normosospermia and meets the standards. However in the residents of the industrial city the ejaculate quality indices were mostly at the lower level of the norm and were significantly worse than in the residents of the control city. Cadmium contained in male biosubstrates affect the hormonal status and quality of semen. Conclusion. Violations of spermatogenesis can serve as a rapidly-responding and reliable criterion for assessing the adaptation and maladaptation processes of men under the influence of xenobiotics of the environment, in particular cadmium. In this case, the markers of influence are the total number of sperm in the ejaculate, their concentration, mobility and the number of pathological forms, semen viscosity
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Oxidative stress has been identified as a major mediator in various etiologies of male infertility. Lead and cadmium are two of the well-known reproductive toxicants to which human are exposed occupationally and environmentally. These heavy metals can lead to negative effects on the testicular functions. The aim of the current study is to look for the differences in the oxidative stress status in serum and seminal plasma of infertile male patients (oligo, azoospermia) groups compared to that of fertile healthy (control) group and to evaluate lead and cadmium levels in sera and seminal plasma of these groups in comparison to fertile healthy controls. The correlation between their level in seminal plasma and serum was also investigated. The current study included three groups of Iraqi male, 32 infertile patients with oligospermia, with 32 infertile patients with azoospermia, and 37 fertile healthy as a control group. The measured parameters included serum and seminal plasma total oxidant status (TOS), total antioxidant capacity (TAC), oxidative stress index (OSI), lead and cadmium concentration. The results in comparison with that of the control groups showed:-1. A highly significant increase differences in serum (TOS), (OSI), Pb, and Cd in 2. serum of all infertile groups and between them. 3. A significant decrease in serum TAC of azoospermia group, as well as a highly 4. significant decrease in serum TAC of oligospermia group with significantdifferences between these two patients groups. 5. No significant differences in seminal plasma TOS, TAC, and OSI in all of the infertile groups. 6. In seminal plasma, a highly significant decrease in Cd and Pb of azoospermia group. Meanwhile a highly significant decrease in Pb of oligospermia group with highly significant differences between them. The results showed no correlation in the measured parameters between serum and seminal plasma of both studied patients. The Pearsonal correlation analysis of TOS, TAC, OSI, Cd, and Pb revealed the presence of:-in oligospermia group, a strong negative correlation was found between serum, (TOS&TAC), and (TAC&OSI), meantime strong positive correlation between ((TOS&OSI) also noticed. In serum azoospermia group a positive correlation between TOS&OSI and negative correlation between TAC &OSI were found. Meanwhile in seminal plasma a negative correlation was found between OSI&TAC. Furthermore, the result revealed, that the non-significant inverse relationship exists between lead and Cadmium concentration in serum and the number of sperm.
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Low-level heavy metals exposure may contribute much more toward the causation of chronic disease and impaired functioning than previously thought. Among the suggested preventive and intervention measures for the control of renal diseases are the reduction in the exposure to heavy metals. Although these indicate knowledge and awareness of possible role of some heavy metals in the etiogenesis of some chronic diseases by Nigerian Physicians, heavy metal assay as diagnostic guide in patient management is often omitted in most healthcare settings. This is a synoptic capture of the increased incidence and prevalence of some metabolic disorders where heavy metals may be implicated. A search of the terms heavy metal exposure, source, toxicity, metabolic disorders, poisoning in Nigeria, in bibliographical databases (in English language) such as PubMed, Scopus, Google Scholar, and Africa Journal Online (AJOL) digital library was conducted. Leaded gasoline, refuse dumping, absence of poison information centers, and poor record keeping characterize environmental health in Nigeria. Lead and cadmium are of most significant public health importance in Nigeria. The recognition and inclusion of heavy metals assays in the diagnosis of metabolic disorders may ensure early diagnosis and improve management.
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Cadmium (Cd) is a widespread environmental toxic contaminant, which causes serious health-related problems. In this study, human intestinal cell line (Caco-2 cells) and normal human liver cell line (HL-7702 cells) were used to investigate the toxicity and bioavailability of Cd to both cell lines and to validate these cell lines as in vitro models for studying Cd accumulation and toxicity in human intestine and liver. Results showed that Cd uptake by both cell lines increased in a dose-dependent manner and its uptake by Caco-2 cells (720.15 µg mg(-1) cell protein) was significantly higher than HL-7702 cells (229.01 µg mg(-1) cell protein) at 10 mg L(-1). A time- and dose-dependent effect of Cd on cytotoxicity assays (LDH release, MTT assay) was observed in both Cd-treated cell lines. The activities of antioxidant enzymes and differentiation markers (SOD, GPX, and AKP) of the HL-7702 cells were higher than those of Caco-2 cells, although both of them decreased significantly with raising Cd levels. The results from the present study indicate that Cd above a certain level inhibits cellular antioxidant activities and HL-7702 cells are more sensitive to Cd exposure than Caco-2 cells. However, Cd concentrations <0.5 mg L(-1) pose no toxic effects on both cell lines.
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The exact causes of the decline in semen quality are not yet known, environmental factors have been considered to play an important role. Lead (Pb) and Cadmium (Cd) are two of the well-known reproductive toxicants to which humans are exposed occupationally and environmentally and can lead to negative effects on the testicular functions. The aim of this study was to evaluate lead and cadmium levels in seminal plasma of men with idiopathic oligoasthenozoospermia in comparison to fertile healthy controls and to correlate these levels with conventional semen parameters, sperm hypo-osmotic swelling (HOS) percentage, sperm DNA fragmentation percentage, and semen reactive oxygen species (ROS) levels. Thirty infertile male patients with idiopathic oligo and/or asthenozoospermia and thirty healthy fertile men, which was the control group, were included in the study. Lead and cadmium levels in seminal plasma, semen parameters, sperm HOS, sperm DNA fragmentation percentage and semen ROS assay were measured in all subjects. There was a significant increase in seminal lead and cadmium levels among infertile males in comparison to controls. There were significant negative correlations between seminal lead and cadmium levels on one hand and certain semen parameters especially progressive sperm motility and vitality (HOS). Importantly, significant positive correlations were noted between seminal lead and cadmium levels on one hand and sperm DNA fragmentation percentage and semen ROS level in infertile men and controls on the other hand. Thus, men with idiopathic male infertility had higher levels of lead and cadmium in their semen which correlated with impairment of sperm motility and vitality percentages and more importantly with higher sperm DNA fragmentation% and semen ROS level.
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To assess if they were within the safety limits for human consumption, the Cd, Cu, Pb, and Zn contents of fish muscles, bought from separate stalls of the fish markets of nine cities of NW Mexico, were determined by atomic absorption spectrophotometry. Considering all fish and markets, the mean contents were Zn: 23.23 ± 5.83, Cu: 1.72 ± 0.63, Cd: 0.27 ± 0.07, and Pb: 0.09 ± 0.04 µg/g (dry weight). Cu, Zn, and Pb did not reach levels of concern for human consumption, but the high Cd values determined in Mazatlán (Mugil cephalus: 0.48 ± 0.15; Diapterus spp.: 0.57 ± 0.33; Lutjanus spp.: 0.72 ± 0.12; small shark: 0.87 ± 0.19 µg/g dry weight) indicate that this was the only metal of concern for human health because the daily individual consumption of fish muscle to reach the PTDI would be within 0.27 and 0.41 kg.
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The influence of dietary cadmium on gonads’ maturation, reproduction and development of offspring of red tilapia was evaluated. The study was conducted on four groups of juvenile red tilapia (average length 8.2 ± 2.5 cm and average weight 38.3 ± 2.5 g). Four doses of cadmium were applied in the feed: 0 mg Cd g−1 (control group), 0.25, 0.5 and 1 mg Cd g−1 of feed (wet weight). The highest dose of Cd (1 mg Cd g−1) inhibited spawning of females, impaired ovarian development. Separation of follicular membrane from underlying ooplasm and abnormal vacuolization of ova were observed. Also in males this dose caused degeneration of spermatogenic elements, fibrosis of lobule walls and blood infiltration. A significant decrease in sperm number and sperm motility was also detected. Cadmium doses of 0.25 and 0.50 mg Cd g−1 did not influence gonads’ development of the studied fish. Ovaries and testis showed no differences in the development between the control group and groups receiving these doses of Cd. However, these doses caused decrease in spawned eggs number, hatchability percentages and increased fries abnormalities. Also, the growth of the developing offsprings was affected by these dietary doses.
In this work, the efficiency of activated carbon derived from carbonized date pits (ADP) and rice husks (ARH) was compared with commercial activated carbon (CAC) for the reduction of COD in wastewater arising from resin manufacturing plant. The process was studied in batch mode with employing different absorbents optimizing various parameters, such as adsorbent dosage, contact time and pH. Adsorption equilibrium and kinetic data were determined for the three adsorbents and were fitted to several isotherm and kinetic models accordingly. The results indicated that a maximum COD reduction of 92.4% was obtained at pH 2 using 30 g/L CAC, 90.3% using 40g/L ADP and 88.9% using 60 g/L ARH. Kinetically, the results data showed that reduction of COD onto the three adsorbents was better fitted to pseudo second-order model. Equilibrium adsorption data for the reduction of COD effluent using CAC, ADP and ARH were best fitted to the Langmuir isotherm model.
Cadmium and zinc have been analyzed in tissues from 292 persons autopsied in Stockholm. In kidney cortex, liver, and pancreas the individual cadmium levels are distributed in a lognormal way. In kidney cortex there is a continuous accumulation of cadmium with age up to 50 years, followed by a decrease. Smokers show a higher cadmium accumulation. For nonsmokers, the biological half time of cadmium in kidney cortex is estimated at 30 years, with m. average concentration at age 50 of 11 μg/g wet weight When smokers are included, the average cadmium concentration at age 50 is 22 μg/g wet weight. Based on the more pronounced cadmium accumulation among smokers than nonsmokers, the respiratory absorption rate of cadmium from tobacco smoke is estimated to be approximately 50%.
In the mammalian testis, the blood–testis barrier (BTB), unlike the blood–brain and blood–retina barriers, is composed of coexisting tight junctions (TJs) and adherens junctions (AJs). Yet these junctions must open (or disassemble) to accommodate the migration of preleptotene and leptotene spermatocytes across the BTB during spermatogenesis while maintaining its integrity. In this report, we show that the BTB utilizes a unique “engagement” and “disengagement” mechanism to permit the disruption of AJ that facilitates germ cell movement without compromising the BTB integrity. For instance, both TJ (e.g., occludin and JAM-1) and AJ (e.g., N-cadherin) integral membrane proteins were colocalized to the same site at the BTB. Although these TJ- and AJ-integral membrane proteins did not physically interact with each other, they were structurally linked by means of peripheral adaptors (e.g., ZO-1 and α- and γ-catenins). As such, these proteins are structurally “engaged” under physiological conditions to reinforce the BTB. When rats were exposed to Adjudin to induce AJ restructuring that eventually led to germ cell loss from the epithelium, this structural interaction between occludin and N-cadherin by means of their adaptors became “disengaged” while their protein levels were significantly induced. In short, when the epithelium is under assault, such as by Adjudin or plausibly at the time of germ cell migration across the BTB during spermatogenesis, the TJ- and AJ-integral membrane proteins can be disengaged. Thus, this mechanism is used by the testis to facilitate AJ restructuring to accommodate germ cell migration while maintaining the BTB integrity. • spermatogenesis • ectoplasmic specialization • Sertoli–germ cell interaction