Synergistic effects of arsenic and fluoride on oxidative stress and apoptotic pathway in Leydig and Sertoli cells

Aydın, Yasemin; Orta-Yilmaz, Banu

doi:10.1016/j.tox.2022.153241

Cited by 15 publications

(3 citation statements)

References 48 publications

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“…Leydig cell morphometry and functionality are disrupted after arsenic exposure through oxidative damage and the subsequent activation of apoptotic pathways. This metalloid also affects the regulation of pituitary gland function with a subsequent reduction in LH and FSH secretion ( Kim and Kim, 2015 ; Zeng et al, 2018 ; Ommati et al, 2019 ; Aydin and Orta-Yilmaz, 2022 ; Machado-Neves, 2022 ).…”

Section: Arsenic Disrupts Male Reproductive Functionsmentioning

confidence: 99%

Arsenic exposure and its implications in male fertility

Machado‐Neves

2022

Anim. Reprod.

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Arsenic exposure is a global health concern. This toxic metalloid is ubiquitous in the environment and contaminates food and drinking water. Once ingested, it undergoes a complex metabolic process within the body, which contributes to its accumulation and reactivity. Arsenic toxicity stems from the induction of oxidative stress, inhibition of thiol-containing proteins, and mimicry of inorganic phosphates. Arsenic poisoning is associated with the development of reproductive disorders. In males, arsenic causes a reduction in testicular weight and alterations in steroidogenesis and spermatogenesis. Moreover, it reduces the number and quality of spermatozoa harvested from the cauda epididymis. The mitochondria are targets of arsenic toxicity because of the production of free radicals and their high content of cysteine-rich proteins and fatty acids. Mitochondrial dysfunction may contribute to reproductive disorders because this organelle is crucial for controlling testicular and epididymal events related to sperm production and maturation. All of these alterations mediated by arsenic exposure contribute to the failure of male reproductive competence by reducing gamete viability. This review describes the potential mechanisms of arsenic toxicity, its detrimental effects on male reproductive organs, and consequences on sperm fertility.

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Section: Arsenic Disrupts Male Reproductive Functionsmentioning

confidence: 99%

Arsenic exposure and its implications in male fertility

Machado‐Neves

2022

Anim. Reprod.

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“…Research indicates that chronic fluoride exposure results in severe hepatocellular vacuolation, and damage to the rough endoplasmic reticulum and mitochondria of hepatocytes, affecting liver metabolism, diminishing hepatic detoxification capacity, and causing varying degrees of injury [3][4][5]. Elevated fluoride intake may lead to intestinal mucosal damage, triggering inflammatory responses in the intestine and impacting intestinal microbiota, resulting in gut dysbiosis [6][7][8]. Prolonged excessive fluoride intake can inflict severe damage on the liver and intestines.…”

Section: Introductionmentioning

confidence: 99%

Bifidobacterium Relieved Fluoride-Induced Hepatic and Ileal Toxicity via Inflammatory Response and Bile Acid Transporters in Mice

Wu,

Cheng,

Wang

et al. 2024

Foods

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Fluoride is a pervasive environmental contaminant. Prolonged excessive fluoride intake can inflict severe damage on the liver and intestines. Previous 16S rDNA sequencing revealed a decrease in ileal Bifidobacterium abundance during fluoride-induced hepatointestinal injury. Hence, this work aimed to investigate the possible mitigating function of Bifidobacterium on hepatointestinal injury caused by fluoride. Thirty-six 6-week-old C57BL/6J mice (equally divided between males and females) were allotted randomly to three groups: Ctrl group (distilled water), NaF group, and NaF + Ba group (100 mg/L NaF distilled water). After 10 weeks, the mice were given 1 × 109 CFU/mL Bifidobacterium solution (0.2 mL/day) intragastrically in the NaF + Ba group for 8 weeks, and the mice in other groups were given the same amount of distilled water. Dental damage, bone fluoride content, blood routine, liver and intestinal microstructure and function, inflammatory factors, and regulatory cholic acid transporters were examined. Our results showed that fluoride increased glutamic-oxalacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT) activities, and the levels of lipopolysaccharide (LPS), IL-1β, IL-6, TNF-α, and IL-10 levels in serum, liver, and ileum. However, Bifidobacterium intervention alleviated fluoride-induced changes in the above indicators. In addition, Bifidobacterium reduced the mRNA expression levels of bile acid transporters ASBT, IBABP, OST-α, and OST-β in the ileum. In summary, Bifidobacterium supplementation relieved fluoride-induced hepatic and ileal toxicity via an inflammatory response and bile acid transporters in the liver and ileum of mice.

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“…Histopathological examination of the liver tissues of the furan-treated groups revealed many lesions, particularly in the higher-dose group. Furan was discovered by (Aydin et al, 2023) to lower the activity of antioxidant enzymes while raising the rates of apoptotic cells, reactive oxygen species, and lipid peroxidation. It also negatively impacts the skin, liver, kidneys, immunological system, neurological system, and fat tissue.…”

Section: Introductionmentioning

confidence: 99%

Glutathione's antioxidant effects and its ability to shield mice's hepatocytes from damage caused by furan

Ibrahim,

Saleh,

Hamouda

2024

Food Technology Research Journal

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Furan is commonly found in several kinds of heat-treated foods, the existence of furan in food causes public health issues. The current research examines the preventive impact of glutathione on liver, kidney function, and tumor markers against furan-induced injury in mice. Male albino mice were divided into seven groups: a control (G1), G2 (0.5mg furan/ kg b.w./day), G3 (1 mg furan/kg b.w./day), G4 (2 mg furan/kg b.w./day), G5 (4 mg furan/ kg b.w./day), G6 (2 mg furan/kg b.w./day +500 mg glutathione/kg/day), and G7 (4 mg furan/kg b.w./day +500 mg glutathione/kg/day). At the end of the study, after 8 weeks, the anesthetized and sacrificed were done, and then the different tests were conducted. Results: Furan significantly increased hepatocyte damage in mice, as evidenced by increased activities of aminotransferase (AST) and alanine aminotransferase (ALT) after a 2mg/kg/ day dose. Furan promoted oxidative stress due to elevated malondialdehyde levels, occurring at various furan dosages (0.5, 1, 2, and 4mg/kg/day). The study found that pretreatment with glutathione at 500 mg/kg/day reduced AST, ALT, and MDA activities in mice, while furan levels did not negatively impact kidney functions. It should be noted that all levels of furan increased tumor markers [Alpha Fetoprotein (AFP)] compared to the control (3.1 ng/ml), whereas glutathione reduced the level of AFP in groups taking furan at (2 and 4 mg/kg) to range (3.5-3.6 mg/ml) compared to (4.6-4.8 mg/ml) for the same groups taking furan at (2 and 4 mg/kg) without glutathione. Glutathione's protective effects against furan-induced hepatocyte damage may be due to its exceptional capacity to scavenge free radicals. Glutathione, with its strong antioxidant properties, has the potential to be a promising therapeutic and preventive agent for diseases induced by furan compounds.

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Synergistic effects of arsenic and fluoride on oxidative stress and apoptotic pathway in Leydig and Sertoli cells

Cited by 15 publications

References 48 publications

Arsenic exposure and its implications in male fertility

Arsenic exposure and its implications in male fertility

Bifidobacterium Relieved Fluoride-Induced Hepatic and Ileal Toxicity via Inflammatory Response and Bile Acid Transporters in Mice

Glutathione's antioxidant effects and its ability to shield mice's hepatocytes from damage caused by furan

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