Chronic chromium exposure-induced changes in testicular histoarchitecture are associated with oxidative stress: Study in a non-human primate (Macaca radiata Geoffroy)

Department of Endocrinology, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, India.
Human Reproduction (Impact Factor: 4.57). 11/2005; 20(10):2801-13. DOI: 10.1093/humrep/dei148
Source: PubMed

ABSTRACT 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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Available from: Subramanian Senthivinayagam, Sep 25, 2015
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    • "Reproductive toxicity of hexavalent chromium [Cr (VI)] in mammals including human beings has recently been reported. Chromium (VI)-induced testicular as well as ovarian toxicity has been demonstrated in laboratory mammals (Murthy et al., 1996; Elbetieha and Al-Hamood, 1997; Aruldhas et al., 2005; Acharya et al., 2006; Subramanian et al., 2006). A few reports correlated chronic occupational chromium exposures to abnormal semen quality in men (Li et al., 2001; Danadevi et al., 2003; Kumar et al., 2005). "
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    ABSTRACT: Exposure to sublethal hexavalent chromium (as 2 and 4 mg L⁻¹ potassium dichromate for 1 and 2 months) during late preparatory to mid prespawning phase of annual reproductive cycle severely affected the pituitary-ovarian axis of a teleost Channa punctatus. Gonadosomatic index (GSI), ovarian histopathology, immunocytochemistry of the pituitary gonadotrophs (LHβ-immunoreactive cells), and serum 17β-estradiol level revealed distinct dose and duration-dependent effects. Gonadosomatic index was declined. Diameter of ovary as well as ovarian follicles was reduced along with a distinct variation in the percentage of follicles. The greater percentage of previtellogenic follicles (stage I) and decline in vitellogenic ones (stage II and stage III) compared to control indicated the arrest of follicular development. The percentage of atretic follicles was also increased indicating toxic impact of metal on ovary. Decreased serum level of ovarian steroid 17β-estradiol further indicated the same. Chromium interference of the pituitary was demonstrated as atrophy and less immunointensity of LH-immunoreactive gonadotrophs. Thus, the hexavalent chromium impaired the pituitary-ovarian axis affecting at the sites of both pituitary and ovary.
    Environmental Toxicology 07/2012; 27(7):415-22. DOI:10.1002/tox.20654 · 3.20 Impact Factor
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    • "Withdrawal of Cr treatment for 6 months normalized spermatogenesis in the testis. It was proven therefore that Cr (VI) disrupts spermatogenesis by inducing free radical toxicity (Aruldhas et al., 2005). "
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    ABSTRACT: Over the past 30 years joint replacement prostheses have been developed and refined to enhance durability and reproducibility. Total hip joint arthroplasty is being performed in an increasing number of younger patients; therefore orthopaedic surgeons seek implants with a longer life span. With regards to the progress of mechanical behaviour of the biomaterials used in an arthroplasty, little is known about the long-term biological effects of wear debris. Owing to the composition of the prostheses currently in use, systemic exposure to chromium (Cr), cobalt (Co), nickel (Ni) and aluminium (Al) alloys occurs as a result of the formation of metal wear nano-particles that are released both from metal-on-metal and polyethylene-on-metal bearings, resulting in a postoperative increase in metal ion levels at different organ sites. These particles circulate both locally and systemically, penetrate cell plasma membranes, bind to cellular proteins and enzymes and modulate cytokine expression. Their physiologic effects are poorly understood and their potential toxicity, hypersensitivity and carcinogenicity remain a cause for concern. In this article we will address the issue of whether these nanoscale degradation products are associated with adverse, clinically significant local or systemic toxicologic sequelae.
    Journal of Applied Toxicology 04/2012; 32(4):255-69. DOI:10.1002/jat.2729 · 2.98 Impact Factor
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    • "Yet, germ cells are continually affected detrimentally by endogenous and exogenous agents, such as reactive oxygen species (ROS), which can cause DNA damage. Spermatozoa were found to be highly sensitive to ROS-induced damage (Aitken and Clarkson 1987), while spermatogonia are reportedly tolerant to ROS (Aruldhas et al. 2005). Previous studies revealed that in mice exposed to mild heat stress, which can consequently lead to oxidative stress (Paul et al. 2009), numerous apoptotic late-type germ cells were found while apoptotic spermatogonia were rare (Paul et al. 2008). "
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