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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
62
Cadmium and male infertility
Alaee S
1*
, Talaiekhozani A
2,3
, Rezaei S
4
, Alaee K
5
, Yousefian E
6
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
Abstract
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
mmm
*
Corresponding Address: Dr. Sanaz Alaee, School
of Advanced Medical Sciences and Technologies,
Shiraz University of Medical Sciences, Shiraz, Iran.
Email: sanazalaee@yahoo.com
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
63
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
problems.
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
(34).
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
64
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-
testic
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,
56).
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
conditions.
Table 1. Studies about effects of cadmium on weight of testes, accumulation of cadmium in testes and plasma
testosterone level.
Model of
research
Cadmium
administration
method
Doses of
cadmium
Duration
of
treatment
Weight of
testes
Accumulation
of cadmium in
testes
Plasma
testosterone
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)
Adult
BALB/c male
mice
Orally
administration
by gavage
CdCl
2,
23 mg/kg
BW 45 days NS Decrease NS Increase S Decrease (15)
CdCl
2,
50 mg/kg
BW once per day S Decrease S Increase S Decrease
Adult Wistar
male rats Orally CdCl
2
(0.2
mg/kg) 15 days NE S Increase S Decrease (21)
Adult Wistar
male rats
Cadmium-
contaminated
radish bulb
1.1 µg Cd/g of
diet
4 weeks No change S Increase NS Increase
(29)
8 weeks No change S Increase S Increase
12 weeks No change S Increase NS Decrease
Adult
Sprague
Dawley male
rats
Subcutaneously 0.6 mg Cd/kg
once per day 6 weeks No Change S Increase NE (31)
Adult
Sprague
Dawley male
rats
Orally,
administration
by gavage
CdCl
2
, 5 mg/kg
BW 15 days S Decrease NE NE (33)
Adult Swiss
Webster male
mice
Intraperitoneal
injection once a
day
CdCl
2,
0.1 mg/kg
BW once per
week
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,
60).
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
65
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
research
Cadmium
administration
method Doses of cadmium Duration
of
treatment Sperm count Sperm motility Reference
Adult Wistar
male rats
Subchronic exposure
to CdCl
2
40 mg/l, per os 30 days S Decrease S Decrease (14)
Adult BALB/c
male mice Orally administration
of CdCl
2
23 mg/kg BW, once per
day 45 days NS Decrease NS Decrease (15)
50 mg/kg WB, once per
day
45 days S Decrease S Decrease
Adult Wistar
male rats Oral administration of
CdCl
2
(0.2
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
(29)
8 weeks NS Decrease NE
12 weeks S Decrease NE
Adult Sprague
Dawley male
rats
Subcutaneous
injection 0.6 mg Cd/kg once per day 6 weeks S Decrease in
testicular SG
and SC NE (31)
Adult Sprague
Dawley male
rats
Oral administration of
CdCl
2
5 mg/kg BW 15 days S Decrease S Decrease (33)
Adult male rats CdCl
2
,
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
C
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
66
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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... 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 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). ...
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... 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). ...
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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%.
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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