In utero Exposure to Atrazine Disrupts Rat Fetal Testis Development

Fang, Yinghui; Ni, Chaobo; Dong, Yaoyao; Li, Huitao; Wu, Siwen; Li, Xiaoheng; Lv, Yao; Huang, Tongliang; Lian, Qingquan; Ge, Ren‐Shan

doi:10.3389/fphar.2018.01391

Cited by 13 publications

(6 citation statements)

References 36 publications

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“…[ 80 ] On the contrary, the GLP‐exposed group revealed a strong immune reaction for PCNA in the nuclei of all spermatogenic cells. This is in agreement with the observations of Fang et al, [ 81 ] who orally administered atrazine, a widely used herbicide, to pregnant rats until the point of birth, at doses of 25, 50, and 100 mg/kg body weight. However, this finding disagreed with those of Yuksel et al, [ 82 ] who orally administered lindane, a widely used pesticide, at daily doses of 10, 20, and 40 mg/kg for 30 days.…”

Section: Discussionsupporting

confidence: 93%

Ameliorative effect of N‐acetylcysteine on the testicular tissue of adult male albino rats after glyphosate‐based herbicide exposure

Hashim

Bashir

Yasin

et al. 2022

J Biochem & Molecular Tox

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Glyphosate (GLP) is a broad-spectrum herbicide that is frequently used in crop production, but its residues remain in foodstuffs. This, in turn, has led to potential adverse effects on both human and animal health. Recent studies emphasized that GLP induces teratogenic effects and reproductive disorders, but its mechanism of toxicity is highly debated. N-acetylcysteine (NAC) is well known for its potent antioxidant capacity in addition to anti-inflammatory and cytoprotective properties.Therefore, our study aimed to investigate the reproductive toxicity of GLP in mature rats and evaluate the possible ameliorative effect of NAC against this toxicity. To this end, 30 adult male rats were assigned into three groups (10 rats per group) as follows: Group I, negative control; group II, GLP-exposed; 375 mg/kg GLP, orally; group III, NAC-cotreated, 160 mg/kg NAC 1 h before GLP, plus GLP, 375 mg/kg orally for 6 weeks. At the end of the experiment, the testicles were collected for semen analysis and biochemical, histopathological, and immunohistochemical studies. GLP-exposed rats exhibited disturbances in seminal parameters and a significant increase in malondialdehyde levels and expression of apoptotic markers. Several histopathological changes were observed, including strong immunoreactions for caspase-3 and proliferating cell nuclear antigen. Conversely, the administration of NAC before GLP was able to improve seminal parameters, attenuate the induced oxidative stress and apoptosis in addition to the regeneration of testicular damage.In conclusion, NAC can ameliorate the reproductive toxicity induced by GLP to an acceptable degree.

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Section: Discussionsupporting

confidence: 93%

Ameliorative effect of N‐acetylcysteine on the testicular tissue of adult male albino rats after glyphosate‐based herbicide exposure

Hashim

Bashir

Yasin

et al. 2022

J Biochem & Molecular Tox

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“…These effects are evident in vivo in amphibians (16) and rats (20), as well as in vitro in human oestrogensensitive tissues (23). Imbalances in these hormones can have a direct effect on the physiology of reproductive organs (24), and exposure to atrazine has caused aggregation and increases in foetal Leydig cell number leading to reduced serum testosterone in post-pubertal males (25), delayed pubertal onset (19), alterations to hormone levels (24,26), and reduced sperm viability in male rodents (19,24,25,27).…”

Section: Introductionmentioning

confidence: 99%

Chronic Atrazine Exposure Beginning Prenatally Impacts Liver Function and Sperm Concentration With Multi-Generational Consequences in Mice

2020

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Atrazine is a commonly used herbicide frequently detected in waterways and drinking water around the world. Worryingly, atrazine is an endocrine and metabolic disruptor but there is a lack of research regarding the effects of long-term exposure beginning in utero. In this study we investigated how chronic exposure to atrazine (5 mg/kg bw/day) in drinking water from E9.5 until 12 or 26 weeks of age affected metabolic and reproductive characteristics in male mice. We then examined whether mating these males to unexposed females altered in vitro embryo characteristics. Atrazine exposure caused a decrease in liver weight and changes in both liver and testis gene expression, specifically in genes involved in lipid uptake and fatty acid metabolism in the liver, as well as androgen conversion in the testis. Notably, atrazine exposure decreased epididymal sperm concentration and subsequent embryo cell numbers generated from the 12-week cohort males. Collectively, these data suggest that atrazine exposure, beginning prenatally, affects both metabolic and reproductive characteristics, and highlights the importance of assessing atrazine effects at different life stages and over multiple generations. The continued widespread use of atrazine warrants further studies, as it is essential to understand the health risks for all species, including humans.

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“…The phenotypes we observed, that is, stunted growth of glans penis and induction of hypospadias in prenatally ATZ‐exposed male mice, and the finding of reduced AR nuclear translocation in developing male GT, consistently suggest that prenatal ATZ exposure disrupts genomic androgen activation during male reproductive organ development. Inhibition of steroidogenesis by ATZ has been reported in peripubertal males and male fetuses in rats (Fang et al, 2018; Trentacoste et al, 2001). However, little is known about the effect of prenatal ATZ exposure on androgen levels in pregnant dams.…”

Section: Discussionmentioning

confidence: 99%

Prenatal exposure to atrazine induces cryptorchidism and hypospadias in F1 male mouse offspring

Tan

Wang

et al. 2021

Birth Defects Research

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The main objective of the present study was to determine whether prenatal exposure to atrazine could affect testicle descent and penile masculinization. Atrazine has been demonstrated with a variety of endocrine disrupting activities and reproductive toxicities. However, the effects of prenatal atrazine exposure on male offspring's genital malformation, such as hypospadias and cryptorchidism, remain poorly understood. In this study, pregnant ICR mice were gavaged from gestational day 12.5–16.5 with different doses of atrazine. Although no sign of systemic toxicity was observed in F1 male pups, prenatal exposure to 100 mg/kg/day atrazine affected penile morphology, urethral meatus position and descent of testis, and reduced anogenital distance and penile size in postnatal day 21 F1 male pups. The comparative study with an androgen receptor (AR) antagonist vinclozolin suggested that these effects of atrazine on male genital development may not be through antagonism of AR. The results also revealed that atrazine exposure significantly reduced maternal serum testosterone levels, decreased AR nuclear translocation, and altered the expression levels of developmental gene networks in developing penis of mice. Atrazine exposure also affected the expression of insulin‐like 3 (Insl3) and steroidogenic gene expression in developing reproductive tract. Therefore, our data indicate that prenatal atrazine exposure can induce hypospadias in F1 mice, likely through disruption of testosterone production, decreasing genomic androgen action, and then altering expression of developmental genes during sexual differentiation. Our data also suggest that prenatal atrazine exposure can induce cryptorchidism in F1 mice, possibly through down regulation of Insl3.

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In utero Exposure to Atrazine Disrupts Rat Fetal Testis Development

Cited by 13 publications

References 36 publications

Ameliorative effect of N‐acetylcysteine on the testicular tissue of adult male albino rats after glyphosate‐based herbicide exposure

Ameliorative effect of N‐acetylcysteine on the testicular tissue of adult male albino rats after glyphosate‐based herbicide exposure

Chronic Atrazine Exposure Beginning Prenatally Impacts Liver Function and Sperm Concentration With Multi-Generational Consequences in Mice

Prenatal exposure to atrazine induces cryptorchidism and hypospadias in F1 male mouse offspring

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