Reproductive toxicity of chromium is in dispute despite positive findings in rodents. Recently we reported epididymal toxicity of hexavalent chromium (CrVI) in bonnet monkeys and in this paper we report its testicular toxicity.
Adult monkeys (Macaca radiata) were given drinking water containing CrVI (100, 200, 400 p.p.m.) for 6 months and testes were removed for ultrastructural and biochemical analyses.
CrVI treatment disrupted spermatogenesis, leading to accumulation of prematurely released spermatocytes, spermatids and uni- and multinucleate giant cells in the lumen of seminiferous tubules. Transmission electron microscopy revealed granulation of chromatin and vacuolation between acrosomal cap and manchette microtubules of elongated spermatids and in the Golgi area of round spermatids. Pachytene spermatocytes had fragmented chromatin and swollen mitochondria with collapsed cristae. Spermatocytes and spermatogonia in the basal compartment were unaffected. Macrophages containing phagocytosed sperm and dense inclusions in Sertoli cells were seen. Specific activities of the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase and concentrations of the non-enzymatic antioxidants glutathione, vitamins A, C and E decreased, while concentrations of H(2)O(2) and hydroxyl radicals increased in the testis of chromium-treated monkeys. Withdrawal of chromium treatment for 6 months normalized spermatogenesis and the status of pro- and antioxidants in the testis.
CrVI disrupts spermatogenesis by inducing free radical toxicity, and supplementation of antioxidant vitamins may be beneficial to the affected subjects.
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"Because several antioxidants are needed to protect against ROS and antioxidant defense may respond differently depending on species, previous studies have shown that the measure of the levels of antioxidant molecules could be interesting biomarkers of pollutant exposure (Berglund et al., 2007; Koivula and Eeva, 2010). It has also been shown that oxidative stress toxicity caused by xenobiotics intoxication affected fertility (Aruldhas et al., 2005). The pollution of living environment in Gabès, one of the most remarkable pollution hotspots in North Africa and the Mediterranean (Azri et al., 2002aAzri et al., , 2002b), presents an ecological problem because of the installation in the early 1970s of intense phosphate treatment industries for acid and fertilizer production in the Gabès–Ghannouche factory complex. "
[Show abstract][Hide abstract]ABSTRACT: Air pollution is a threat for human health and wildlife. The aim of this study is to assess the pathophysiological changes and the oxidative–antioxidative status in testicular tissues of 40 Hybrid sparrows collected from four areas in Gabès city, one of the most polluted areas in Tunisia. The testis histopathological analysis revealed alterations in birds from Ghannouche, the polluted area. The thiobarbituric acid reactive substance (TBARS) levels were higher in testis of birds from the contaminated site compared to less polluted areas indicating oxidative damage to membrane lipids. Antioxidant enzyme activities (superoxide dismutase and catalase) were lower in testis sparrows from the polluted site compared with the reference site, suggesting deficiency of the antioxidant system to compensate for oxidative stress. Overall, our results suggest that the hybrid sparrow offers a suitable model for biomonitoring programs of atmosphere pollutants and the selected biomarkers could be useful tool to evaluate pollution impacts in living organisms.
Full-text · Article · Mar 2016 · Ecotoxicology and Environmental Safety
"Nephrotoxicity is a major adverse effect of Cr poisoning due to the fact that the main known route for chromium excretion is through the kidney with a resultant increase in its chromium content and subsequently, nephropathy . The toxic manifestations of Cr are attributed primarily to oxidative stress [5,6] leading to serious damage to the vital organs [7,8]. The role of inflammation in acute kidney injury (AKI) has been increasingly appreciated with involvement of leukocytes, adhesion molecules, chemokines, and cytokines. "
[Show abstract][Hide abstract]ABSTRACT: Hexavalent chromium (CrVI) is a heavy metal widely used in more than 50 industries. Nephrotoxicity is a major adverse effect of chromium poisoning. The present study investigated the potential renoprotective effect of lactoferrin (Lf) against potassium dichromate (PDC)-induced acute kidney injury (AKI) in rats. Beside, because previous studies suggest that interlukin-18 (IL-18) and insulin-like growth factor-1 (IGF-1) play important roles in promoting kidney damage, the present work aimed to evaluate the involvement of these two cytokines in PDC model of AKI and in the potential renoprotective effect of lactoferrin. Adult male albino Wistar rats were pretreated with Lf (200mg/kg/day, p.o.) or (300mg/kg/day, p.o.); the doses that are usually used in the experiment studies, for 14 days followed by a single dose of PDC (15mg/kg, s.c.). PDC caused significant increase in serum urea, creatinine, and total protein levels. This was accompanied with decreased renal glutathione content, and increased renal malondialdehyde, IL-18, IL-4, nuclear factor kappa B (NFκB), IGF-1, and the phosphorylated form of forkhead box protein O1 (FoxO1) levels. Moreover, normal expression IFN-γ mRNA and enhanced expression of TNF-α mRNA was demonstrated in renal tissues. Histopathological investigations provoked deleterious changes in the renal tissues. Tubular epithelial hyperplasia and apoptosis were demonstrated immunohistochemically by positive proliferating cell nuclear antigen (PCNA), Bax, and Caspase-3 expression, respectively. Pretreatment of rats with Lf in both doses significantly corrected all previously mentioned PDC-induced changes with no significant difference between both doses. In conclusion, the findings of the present study demonstrated the involvement of oxidative stress, inflammatory reactions, tubular hyperplasia and apoptosis in PDC-induced AKI. It suggested a role of IL-18 through stimulation of IL-4-induced inflammatory pathway, and IGF-1 through triggering FoxO1-induced cell proliferation. Moreover, the study revealed that Lf protected the kidney against Cr-induced AKI in rats and significantly showed antioxidant, anti-inflammatory, and anti-proliferative properties with down-regulation of IL-18 and IGF-1.
"Several studies reported OS as a common cause of infertility and altered spermatogenesis in men (Tremellen, 2008; Turner and Lysiak, 2008; Aruldhas et al., 2005). The objectives of our study were to examine OS-related biochemical aspects, essential metals and androgenic status, as well as morphological changes of the testes of male Wistar rats subacutely intraperitoneally (i.p.) exposed to Cd. Focusing on testicular toxicity of Cd, we assessed OS by measuring superoxide anion radical (O 2 À ), activities of total SOD and GST; CAT; lipid peroxidation (LPO); reduced glutathione (GSH) and oxidized glutathione (GSSG); the status of certain biometals [zinc (Zn), copper (Cu), iron (Fe) and magnesium (Mg)]; and testosterone level in the testes. "
[Show abstract][Hide abstract]ABSTRACT: The objective of our study was to examine testicular toxicity of cadmium (Cd), focusing on oxidative stress (OS), essential metals and androgenic status and morphological changes. Male Wistar rats [controls and four Cd-subgroups (n = 6) organized according to the exposure (1, 3, 10 and 21 days)] were intraperitoneally (i.p.) treated with 1 mg CdCl2/kg/day. Testicular Cd deposition was noticed from the 1st day. After 10 and 21 days, copper (Cu) and iron (Fe) increased by 60-109% and 43-67%, respectively, while zinc (Zn) decreased by 24-33%. During 1-21 days of the exposure, decrease in testicular total superoxide dismutase (SOD) and total glutathione-s-transferase (GST) activities occurred gradually by 30-78% and 15-84%, respectively, while superoxide anion radical (O2-) increased gradually by 114-271%. After 10-21 days, decrease in testicular catalase (CAT) activity appeared by 13-31%. After 21 days, malondialdehyde (MDA) decreased by 44% and the ratio of oxidized glutathione/reduced glutathione (GSSG/GSH) increased by 130% in testes of the rats exposed to Cd. Additionally, decreased testicular testosterone level and the relative testes mass, along with induced microscopic and macroscopic changes were occured, what can be explained as the consequence of instantly developed OS, impaired essential metals status and Cd testicular deposition.
Full-text · Article · Sep 2015 · Food and Chemical Toxicology