Testicular toxicity of profenofos in matured male rats

Moustafa, Gihan G.; Ibrahim, Zein Shaban; Hashimoto, Yoshiharu; Alkelch, Alkelch M.; Sakamoto, Kentaro Q.; Ishizuka, Mayumi; Fujita, Shoichi

doi:10.1007/s00204-007-0217-2

Cited by 39 publications

(19 citation statements)

References 20 publications

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“…CCl4-treated group showed sloughing and destruction of walls of seminiferous tubules necrosis, edema, and increase in fibers deposition (Figs. 21, 22, and 23), in accordance with Manierea et al (2005); Moustafa et al (2007)); Manjrekar et al (2008); Khan and Ahmed (2009);Hanafi (2012), and Khan (2012). These effects are due to the production of oxygen radicals in excess of the antioxidant capacity of the stressed tissue Yousef and Salama (2009).…”

Section: Resultsmentioning

confidence: 87%

The protective effect of N-acetyl cysteine against carbon tetrachloride toxicity in rats

Foaud

Kamel

El-Monem

2018

JoBAZ

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Background: Carbon tetrachloride (CCL4) is used as a solvent for oils and fats, as a refrigerant, and as a dry-cleaning agent. Inhalation of its vapors can depress central nervous system activity and cause degeneration of the liver and kidneys. Aim: The aim of this study was to investigate whether N-acetyl cysteine (NAC) has a protective effect on the toxicity caused by carbon tetrachloride. Methods: Male rats were used in this experiment. Animals were divided into five groups, 5 animals each: G1 received olive oil, G2 was treated with CCL4 (1 ml/kg body wt) dissolved in olive oil (1:1), G3 received NAC (300 mg/kg body wt), G4 received CCL4 plus NAC, and G5 received NAC for 1 week then administrated to the same treatment of G4. All administrations were performed by gavage and maintained for 4 weeks. Results: The present study revealed that administration of CCL4 caused a significant increase in liver marker enzymes Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), and alkaline phosphatase (ALP); also, malondialdehyde (MDA) content in the liver tissue was increased. However, serum total protein showed no change in all groups. Also, histopathological investigation of CCL4 on the liver, testis, and kidney showed different deleterious effects. Additionally, CCl4 induced a highly significant increase in the percentage of sperm shape abnormality and sperm DNA tail moment values. Alternatively, result revealed that the two routes of NAC administrations caused a significant decrease in liver marker enzymes as well as MDA contents; improvement in liver, kidney, and testes architecture; a significant decrease in the percentage of sperm head abnormalities; and decline in the DNA tail moment values. Conclusion: The present study pointed out the protective effect of NAC against the toxicity of CCL4.

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Section: Resultsmentioning

confidence: 87%

The protective effect of N-acetyl cysteine against carbon tetrachloride toxicity in rats

Foaud

Kamel

El-Monem

2018

JoBAZ

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“…These pesticides caused spermatozoa dysfunctions due to their cumulative GroupIII(profenofos+selenium)(n=6) ng/ml effect or their chronic exposure (Selvaraju et al, 2011). Exposure to OPI may cause endocrine changes both directly (as hormone agonists or antagonists) and indirectly (altering circulating levels of hormones by influencing rates of hormone synthesis or metabolism), which can severely affect steroid hormone actions (Moustafa et al, 2007). Hypertrophy in Leydig cells results, disrupt the functioning of the testes to release testosterone hormone for normal spermatogenesis that creates fertility problems .…”

Section: Pathological Examinationmentioning

confidence: 99%

Protecting Role of Selenium on the Cytotoxic Effect of Profenofos on Rabbit Fertility

Abdel-Rahman¹,

El-Metwally²,

El-Hallawany³

et al. 2017

AJVS

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Key words:Profenofos -Histopathology-Caspase-3 -Biochemical-HormonesAntioxidants-Reproductive toxicity -Selenium-Liverkidneys -Rabbits.Profenofos is an Organophosphorous compound and acaricide used in Egypt with cumulative toxic effects causing reproductive dysfunction and increase in reactive oxygen species production. Protective and anti-oxidant effects of selenium can improve the activity of radical scavenger. So, the aim of this study was to elucidate the protective effects of Selenium against reproductive toxicity induced by Profenofos in male and female New Zealand rabbits (n=18). Three experimental groups (3 males and 3 females per each group) receiving a combination of Profenofos (70 mg/ kg b. w.) and/or selenium in drinking water (25 mg/ kg b. w.) for 90-day was divided as follows: non treated (control), Profenofos alone and Profenofos + selenium group. Profenofos caused a decrease in body and organs weights compared to control group. It had a fetotoxic effect resulting in a significant reduction in pregnancy rate and the number of viable feti in treated animals. Also, Profenofos caused a significant elevation in ALT, AST, MDA, urea and creatinine, while a significant decrease was noticed in SOD, GSH, testosterone, estrogen and progesterone in all treated rabbits compared to control group. Concomitant administration of selenium with Profenofos alleviated the induced alterations. In addition to, histopathological results revealed that testes, epididymis, ovary and uterus alterations represented by degenerative and inflammatory changes as a result of Profenofos exposure. Profenofos had a carcinogenic effect on uterus as leiomyoma with rhabdomyosarcoma which gave positive immunoreactivity with Desmin and Smooth muscle actin. Also, Profenofos caused histopathological and histochemical effects in liver and kidney tissues. There was intensive positive immunoreactivity for caspase-3 (dark brown granules) was observed in the cytoplasm of apoptotic testicular, ovarian and uterine cells that indicating the severity of Profenofos toxicity. On the other hand, examined tissues of Profenofos in combination with selenium treated group showed apparent reduction of caspase-3 immunoreactivity to be more or less similar to the control group. In conclusion, selenium is a valuable cytoprotective which reduced the oxidative stress toxicity induced by Profenofos in the reproductive system of male and female as well as liver and kidney albino rabbits.

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“…The aryl hydrocarbon (dioxin) also increases CYP19A1 (aromatase) expression mediated by its receptor in mouse ovaries [14]. In contrast, the phosphorothioate insecticide profenofos increases the expression of steroidogenic genes and testosterone levels in rat testes [15]. Recently reported adverse effects of BPA on in situ steroidogenesis include increased testosterone levels in mouse Leydig cells and decreased E 2 levels in porcine ovarian granulosa cells [16,17].…”

Section: Introductionmentioning

confidence: 99%

Endocrine Disrupter Bisphenol A Increases In Situ Estrogen Production in the Mouse Urogenital Sinus

Arase

Ishii

Igarashi

et al. 2010

Biology of Reproduction

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The balance between androgens and estrogens is very important in the development of the prostate, and even small changes in estrogen levels, including those of estrogen-mimicking chemicals, can lead to serious changes. Bisphenol A (BPA), an endocrine-disrupting chemical, is a well-known, ubiquitous, estrogenic chemical. To investigate the effects of fetal exposure to low-dose BPA on the development of the prostate, we examined alterations of the in situ sex steroid hormonal environment in the mouse urogenital sinus (UGS). In the BPA-treated UGS, estradiol (E(2)) levels and CYP19A1 (cytochrome P450 aromatase) activity were significantly increased compared with those of the untreated and diethylstilbestrol (DES)-treated UGS. The mRNAs of steroidogenic enzymes, Cyp19a1 and Cyp11a1, and the sex-determining gene, Nr5a1, were up-regulated specifically in the BPA-treated group. The up-regulation of mRNAs was observed in the mesenchymal component of the UGS as well as in the cerebellum, heart, kidney, and ovary but not in the testis. The number of aromatase-expressing mesenchymal cells in the BPA-treated UGS was approximately twice that in the untreated and DES-treated UGS. The up-regulation of Esrrg mRNA was observed in organs for which mRNAs of steroidogenic enzymes were also up-regulated. We demonstrate here that fetal exposure to low-dose BPA has the unique action of increasing in situ E(2) levels and CYP19A1 (aromatase) activity in the mouse UGS. Our data suggest that BPA might interact with in situ steroidogenesis by altering tissue components, such as the accumulation of aromatase-expressing mesenchymal cells, in particular organs.

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Testicular toxicity of profenofos in matured male rats

Cited by 39 publications

References 20 publications

The protective effect of N-acetyl cysteine against carbon tetrachloride toxicity in rats

The protective effect of N-acetyl cysteine against carbon tetrachloride toxicity in rats

Protecting Role of Selenium on the Cytotoxic Effect of Profenofos on Rabbit Fertility

Endocrine Disrupter Bisphenol A Increases In Situ Estrogen Production in the Mouse Urogenital Sinus

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