Arsenic-Induced Sex Hormone Disruption: An Insight into Male Infertility

Choudhury, Birupakshya Paul; Roychoudhury, Shubhadeep; Sengupta, Pallav; Toman, R.; Dutta, Sulagna; Kesari, Kavindra Kumar

doi:10.1007/978-3-031-12966-7_6

Cited by 5 publications

(3 citation statements)

References 71 publications

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“…Consequently, this phenomenon exerts an influence on the spermatogenesis process occurring in the testes as well as the subsequent storage of spermatozoa within the seminiferous tubules. The harmful effects of arsenic are manifested by the stimulation of reactive oxygen species (ROS) generation during redox cycling and metabolic activation mechanisms, resulting in tissue impairment [56]. The deleterious impacts of free radicals on biomembranes are apparent through the observed increase in lipid peroxidation, oxidation of nucleic acids, and degradation of proteins.…”

Section: The Phenolic Compounds Of Salvia Hispanica Seeds Powder (Chia)mentioning

confidence: 99%

Evaluation of Salvia hispanica as a Therapeutic Agent against Sodium Arsenic-Induced Testicular Toxicity in a Male Rats Model

Omar,

Zahran,

Alhotan

et al. 2024

Life

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Chia seeds offer therapeutic properties that aid in the prevention of a variety of ailments, including cardiovascular disease, diabetes, obesity, and other risk factors. Arsenite, a common environmental chemical, has been identified as a reproductive toxin owing to its negative effects on male reproductive health. It has been shown to inhibit spermatogenesis and generate androgenic effects in men. The primary goal of this research was to look into the effect of Salvia hispanica on testicular toxicity caused by sodium arsenite in male rats. A set of 36 male albino rats was allocated to a negative control cohort. The individuals in this group were given a basic meal and orally given distilled water for a duration of 28 days. The other five groups were given a regular meal and received intra-peritoneal injections of sodium arsenite (NaAsO2) at a concentration of 4 mg/kg body weight that was diluted in a 0.9% NaCl solution. The injections were administered consecutively, with two doses given within a two-day period. Subsequently, the rats were categorized into several groups using the following classification: Group 2 consisted of a positive control cohort, in which the rats were given a typical baseline diet. Groups 3, 4, 5, and 6 were given a basic diet that included varying proportions of ground chia seeds, namely 5%, 10%, 15%, and 20% per 100 g of the diet. After the trial was completed, the rats were euthanized, and further biological examination was conducted. The measurements of the reproductive organs were documented and reported. The research assessed the following characteristics: sperm count, motility, progressive motility, and normal morphology. The research included examining serum sex hormones, namely luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone. An evaluation of the activity of antioxidant enzymes was performed in the tissue of the testicles. There were statistically significant improvements in the sperm parameters, serum sex hormone levels, and the activity of antioxidant enzymes, such as GPX, SOD, and CAT, in the therapy groups. The levels of malondialdehyde (MDA) exhibited a noteworthy decrease (p ≤ 0.05) when compared to the positive control group. Salvia hispanica seeds have demonstrated a significant level of effectiveness in reducing sodium arsenite-induced testicular toxicity, which leads to the conclusion. The flavonoid content and antioxidant properties of Salvia hispanica seeds may be to blame for the observed behavior. These indicated characteristics may have therapeutic significance in treating testicular harm induced by arsenite exposure.

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Section: The Phenolic Compounds Of Salvia Hispanica Seeds Powder (Chia)mentioning

confidence: 99%

Evaluation of Salvia hispanica as a Therapeutic Agent against Sodium Arsenic-Induced Testicular Toxicity in a Male Rats Model

Omar,

Zahran,

Alhotan

et al. 2024

Life

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“…Studies conducted with rodents suggest that exposure to inorganic arsenic (e.g., arsenite) impairs reproductive functions in both males and females. Effects in males include a reduction in testicular weight, an imbalance in circulating male sex hormones, and impairment of spermatogenesis and sperm development, leading to low sperm count [ 16 , 17 ]. On the other hand, effects in females include the reduction in circulating female sex hormones, the suppression of ovarian steroidogenesis, prolonged diestrus, the degeneration of reproductive cells (ovarian, follicular, and uterine cells), and an increase in meiotic aberrations in oocytes [ 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Reproductive and Developmental Effects of Sex-Specific Chronic Exposure to Dietary Arsenic in Zebrafish (Danio rerio)

Rachamalla,

Salahinejad,

Kodzhahinchev

et al. 2024

Toxics

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The present study investigated the reproductive and developmental effects of sex-specific chronic exposure to dietary arsenic in zebrafish. Adult zebrafish (Danio rerio) were exposed to environmentally realistic doses of arsenic via diet [0 (control; no added arsenic), 30 (low), 60 (medium), and 100 (high) μg/g dry weight, as arsenite] for 90 days. Following exposure, arsenic-exposed females from each dietary treatment were mated with control males, and similarly, arsenic-exposed males from each dietary treatment were mated with control females. In females, arsenic exposure resulted in a dose-dependent decrease in reproductive performance (fecundity, fertilization success, and hatching success). Moreover, a dose-dependent increase in developmental toxicity (larval deformities and larval mortality) was observed with maternal exposure to arsenic. In contrast, in males, arsenic exposure also induced similar reproductive and developmental toxicity; however, the adverse effects were mainly evident only in the medium and high dietary arsenic treatment groups. We also examined the sex-specific effects of dietary arsenic exposure on the expression of genes that regulate the hypothalamus–pituitary–gonadal–liver (HPG-L) axis in fish. The gene expression results indicated the downregulation of HPG-L axis genes in females irrespective of the arsenic treatment dose; however, the reduced expression of HPG-L axis genes in males was recorded only in the medium and high arsenic treatment groups. These observations suggest that chronic arsenic exposure in either females or males causes reproductive and developmental toxicity in zebrafish. However, these toxic effects are markedly higher in females than in males. Our results also suggest that arsenic can act as an endocrine disruptor and mediate reproductive and developmental toxicity by disrupting the HPG-L axis in zebrafish.

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“…2 induced liver fibrosis are multifaceted, including oxidative stress, inflammatory response, apoptosis, necrosis, and methylation [7][8][9]. In recent years, studies demonstrates that autophagy plays a critical role inarsenic-related carcinogenic mechanisms.…”

Section: Introductionmentioning

confidence: 99%

PTEN Overexpression Alters Autophagy Levels and Slows Sodium Arsenite-Induced Hepatic Stellate Cell Fibrosis

Huang¹,

Ding²,

Yuan³

et al. 2023

Preprint

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Background: Exposure to inorganic arsenic (iAs) remains a global public health problem. The liver is the main target organ of arsenic, leading to arsenic-induced liver fibrosis. Autophagy is involved. Phosphatase and tensin homology deleted on chromosome ten (PTEN) may participate in arsenic-induced liver fibrosis by regulating autophagy, but the exact mechanisms remain unclear. We established a mouse model of arsenic poisoning through the drinking water, and a fibrosis model using the huma stellate cell (HSC) line LX-2, which was exposed to NaAsO2 for 24h. HE and Masson staining was adopted to observe the degree of liver fibrosis. The cells were transfected using PTEN overexpression plasmid. Western blot and qRT-PCR were used to determine the levels of protein/mRNA expression. The in vivo results were confirmed in HSCs exposed to NaAsO2, with changes suggesting fibrosis as seen in mice. NaAsO2 upregulated the expression of the autophagic markers microtubule-associated protein light chain A/B (LC3), recombinant human autophagy effector protein (Beclin-1), hairy and enhancer of split homolog-1 (HES1), but downregulated PTEN. α-smooth muscle actin (α-SMA) expression was significantly upregulated in all NaAsO2 groups. PTEN overexpression altered NaAsO2-induced autophagy which LC3, Beclin-1 were downregulated. Notch1, HES1, α-SMA, and collagenⅠexpression were all downregulated in the NaAsO2 groups. In conclusion, PTEN overexpression might decrease autophagy and inhibit fibrosis progression caused by this toxin. The NOTCH1/HES1 pathway is likely to be involved in this process. Most previous studies did not investigate PTEN and arsenic-induced liver fibrosis specifically. The present study highlights the importance of targeting PTEN for the management of arsenic exposure.

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Arsenic-Induced Sex Hormone Disruption: An Insight into Male Infertility

Cited by 5 publications

References 71 publications

Evaluation of Salvia hispanica as a Therapeutic Agent against Sodium Arsenic-Induced Testicular Toxicity in a Male Rats Model

Evaluation of Salvia hispanica as a Therapeutic Agent against Sodium Arsenic-Induced Testicular Toxicity in a Male Rats Model

Reproductive and Developmental Effects of Sex-Specific Chronic Exposure to Dietary Arsenic in Zebrafish (Danio rerio)

PTEN Overexpression Alters Autophagy Levels and Slows Sodium Arsenite-Induced Hepatic Stellate Cell Fibrosis

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