Male reproductive toxicity of sodium arsenite in mice

Pant, Niraj; Murthy, Ramesh; Srivastava, Sri Prakash

doi:10.1191/0960327104ht467oa

Cited by 129 publications

(85 citation statements)

References 21 publications

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“…This can be supported from the fact that the mice that received SA had lower epdidymidis sperm counts compared to the control mice in our previous study (Chang et al, 2007). For other examples, mice that were continuously exposed to arsenic for 35 days showed decreased sperm counts (Pant et al, 2001). Similarly, in rats, exposed to SA suppressed spermatogenesis (Sarkar et al, 1991(Sarkar et al, , 2003.…”

Section: Discussionsupporting

confidence: 63%

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Decreased Levels of Plasma Testosterone/LH Ratio in Male Mice Exposed to Sodium Arsenite

Chang¹,

Kim²,

Park³

et al. 2010

Biomolecules and Therapeutics

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-While it's been shown that arsenic impairs male reproductive function, it remains unclear whether the mechanism involves an effect on testosterone (T) production. We examined plasma T and luteinizing hormone (LH) levels in mice given water containing either 20 or 40 mg/L sodium arsenite (SA). The plasma T levels were lower in SA-treated mice than in controls and correlated well with testicular T levels within individuals. However, SA treatment did not significantly affect plasma LH levels. The ratio of plasma T to LH was reduced by the treatment with 40 mg/L SA. These results suggest arsenic-induced defect in testicular testosterone production in mice.

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Section: Discussionsupporting

confidence: 63%

“…Arsenic has been found to impair male reproductive function in rats and mice (Sarkar et al, 1991(Sarkar et al, , 2003Pant et al, 2001). In light of those studies, our current data support that arsenic impairs testis function of T production in mice.…”

Section: Discussionmentioning

confidence: 99%

Decreased Levels of Plasma Testosterone/LH Ratio in Male Mice Exposed to Sodium Arsenite

Chang¹,

Kim²,

Park³

et al. 2010

Biomolecules and Therapeutics

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“…Furthermore, a low dose of arsenic (0.1 mM), in the presence of hCG, already significantly suppressed germ cell proliferation. In mammals, reduced sperm count and motility after oral administration of sodium arsenite in mice (Pant et al 2001) and early arrest of spermatogenesis after i.p. administration of sodium arsenite in rats (Ahmad et al 2008) have been observed.…”

Section: Discussionmentioning

confidence: 99%

Arsenic inhibits in vitro spermatogenesis and induces germ cell apoptosis in Japanese eel (Anguilla japonica)

Celino¹,

Yamaguchi²,

Miura³

et al. 2009

Reproduction

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The precise mechanism and direct effects of arsenic on fish, particularly in reproduction, are not well clarified. The aim of this study is to investigate the direct influence of arsenic on fish spermatogenesis using the Japanese eel (Anguilla japonica) in vitro testicular organ culture system. Eel testicular fragments were cultured in vitro with 0.1-100 mM arsenic with or without human chorionic gonadotropin (hCG) for 6 or 15 days at 20 8C. Arsenic treatment provoked a dose-dependent inhibition of hCG-induced germ cell proliferation as revealed by 5-bromo-2-deoxyuridine immunohistochemistry. Time-resolved fluorescent immunoassay showed that arsenic suppressed hCG-induced synthesis of 11-ketotestosterone (11-KT) in testicular fragments incubated with 0.0001-100 mM arsenic and hCG for 18 h. A 0.1 mM (7 mg/l) dose of arsenic which is lower than the World Health Organization drinking water quality guideline of 10 mg/l most effectively reduced 11-KT production. The hCG-induced synthesis of progesterone from pregnenolone was significantly inhibited by low doses of arsenic (0.1-1 mM), implying an inhibition of 3b-hydroxysteroid dehydrogenase activity. In situ TUNEL assays indicated that germ cells undergo apoptosis at the highest dose of arsenic (100 mM). An arsenic concentration-dependent increase in oxidative DNA damage was detected by 8-hydroxy-2 0 -deoxyguanosine (8-OHdG) immunohistochemistry. A peak in 8-OHdG index was observed in testicular fragments treated with 100 mM arsenic and hCG consistent with the TUNEL results. These data suggest that low doses of arsenic may inhibit spermatogenesis via steroidogenesis suppression, while high doses of arsenic induce oxidative stress-mediated germ cell apoptosis.

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“…Mice were treated with drinking water containing arsenite (533.9 mmol/L (69.4 mg/L) for 35 days), the form of arsenic most frequently found in drinking water [Pant et al 2001]. Arsenic levels increased in the testes (0.52 to 5.26 mg/kg, po 0.05), epididymis (2.70 to 4.70 mg/kg, p o0.05), and in the seminal vesicles (po 0.05).…”

Section: Animal and In-vitro Studiesmentioning

confidence: 99%

Adverse Effects of Low Level Heavy Metal Exposure on Male Reproductive Function

Wirth

Mijal

2010

Systems Biology in Reproductive Medicine

223

164

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Lead, cadmium, mercury, and arsenic, often referred to as ''heavy metals'', are toxic for wildlife, experimental animals, and humans. While experimental animal and human occupational studies with high exposure levels generally support an adverse role for these metals in human reproductive outcomes, information on the effects of low, environmentally-realistic exposure levels of these metals on male reproductive outcomes is limited. We review the literature on effects of exposure to low levels of these metals on measures of male fertility (semen quality and reproductive hormone levels) and provide supporting evidence from experimental and occupational studies. Potentially modifying effects of genetic polymorphisms on these associations are discussed. A brief review of the literature on the effects of three trace metals, copper, manganese, and molybdenum, that are required for human health, yet may also cause adverse reproductive effects, follows. Overall, there were few studies examining the effects of exposure to low levels of these metals on male reproductive health. For all metals, there were several well-designed studies with sufficient populations appropriately adjusted for potential confounders and many of these reported harmful effects. However, many studies lacked sufficient numbers of participants to be able to detect differences in outcomes between exposed and non-exposed individuals, did not clearly identify the source and characteristics of the participants, and did not control for other exposures that could alter or contribute to the outcomes. The evidence for the effects of low exposure was strongest for cadmium, lead, and mercury and less certain for arsenic. The potential modifying effects of genetic polymorphisms has not been fully explored. Additional studies on the reproductive effects of these toxic ubiquitous metals on male reproduction are required to expand the knowledge base and to resolve inconsistencies.

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Male reproductive toxicity of sodium arsenite in mice

Cited by 129 publications

References 21 publications

Decreased Levels of Plasma Testosterone/LH Ratio in Male Mice Exposed to Sodium Arsenite

Decreased Levels of Plasma Testosterone/LH Ratio in Male Mice Exposed to Sodium Arsenite

Arsenic inhibits in vitro spermatogenesis and induces germ cell apoptosis in Japanese eel (Anguilla japonica)

Adverse Effects of Low Level Heavy Metal Exposure on Male Reproductive Function

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