Effects of Chronic Ethanol Consumption on Biochemical Parameters and Oxidative Stress on Rat

Mirzaei, Ali; Mirzaei, Nooshin; Alamdari, Ahmad

doi:10.17485/ijst/2015/v8i25/59160

Cited by 6 publications

(3 citation statements)

References 17 publications

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“…Adequate intake of ascorbic acid every day in animal or human leads to an increase in GSH (Waly et al, 2015). Mirzaei et al (2015) study also agreed with our study as it showed that consumption of ethanol in rats after 12 weeks causes a significantly decreased in reduced glutathione concentration in the ethanol-treated group compared to control group, this decrease in GSH level due to the pathogenic role of oxidative stress which presents in chronic ethanol consumption.…”

Section: Discusionsupporting

confidence: 92%

Possiple Protective Role of Ascorbic Acid on Ethanol Induced Testicular Toxicity in Male Albino Rats

Ahmed

Haroun

Hassan

et al. 2019

The Egyptian Journal of Forensic Sciences and Applied Toxicolog

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Background: Exposure to ethanol results in many pathophysiologic changes in the function of the reproductive system caused by the alcohol itself and the effects of its metabolism in recurrent use. Ascorbic acid is a powerful antioxidant that can neutralize harmful compounds and potentiate the antioxidant capacity. Aim: this study was aimed to evaluate the protective effects of ascorbic acid against testicular changes caused by ethanol in adult male albino rats. Materials and Methods: Forty adult male rats were randomly distributed into four groups treated for 63 consecutive days, control group: was treated with distilled water only orally by gastric tube. Ascorbic acid group: was treated with ascorbic acid (100 mg/day/rat) dissolved in distilled water (dilution 50%), once daily orally by gastric tube. Ethanol group: was treated with ethanol (0.7g/kg) dissolved in distilled water (dilution 50% ), once daily orally by gastric tube. Ethanol and ascorbic acid group: was treated with ethanol and ascorbic acid in the same previous doses orally by gastric tube. At the end of the study, rats were weighed then blood samples were obtained from each group to estimate the level of testosterone. Then the rats were sacrificed. The testes were dissected and weighed then used for evaluation of oxidative parameters (GSH and MDA), histopathological examination of testes by light and electron microscope. Results: Concomitant administration of ascorbic acid with ethanol resulted in a highly significant rise in body weight, with increase in mean testosterone level but this rise was insignificant, there was a highly significant decrease in MDA level and there was a highly significant increase in GSH level. Regarding histopathological results in the group of ascorbic acid with ethanol showed improvement in all histopathological changes induced by ethanol. As regard ultrastructure changes, microscopic examination in ethanol group revealed thickening of basement membrane, mitochondrial changes, degenerated spermatid with distorted acrosomal cap, with decrease in the sperm count results which were improved in the group of ascorbic acid with ethanol. Conclusion: oral administration of ethanol daily (50% dilution) for 63 consecutive days in adult albino rats caused various testicular lesions which were significantly reduced with combined administration of ascorbic acid as an antioxidant.

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Section: Discusionsupporting

confidence: 92%

Possiple Protective Role of Ascorbic Acid on Ethanol Induced Testicular Toxicity in Male Albino Rats

Ahmed

Haroun

Hassan

et al. 2019

The Egyptian Journal of Forensic Sciences and Applied Toxicolog

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“…Moreover CBZ induces aneuploidy. In vivo studies revealed that oral administration of CBZ at 50 mg/kg bw in rats [81,83] and 20 mg/kg bw intradermal in rats, [82] induces liver toxicity by Lungs Human Cell culture -4.09-1046.4 µM [28] Placenta Human Cell culture -1, 2.5, 5 µM [27] elevating levels of liver biochemical markers alanine aminotransferase (ALT), aspartate aminotransferases (AST) and alkaline phosphatase (ALP) resulting in hepatocyte damage. CBZ reduces GSH level and inhibited antioxidant enzymes (SOD, CAT) in liver, significantly increased inflammatory and LPO indicators as well as dramatically elevated NO and H 2 O 2 level and MPO activity in rats upon oral exposure to 50 mg/kg bw CBZ.…”

Section: Hepatotoxicitymentioning

confidence: 99%

Carbendazim toxicity in different cell lines and mammalian tissues

Sharma

Maheshwari

Khan

et al. 2022

J Biochem & Molecular Tox

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The extensive production and use of harmful pesticides in agriculture to improve crop yield has raised concerns about their potential threat to living components of the environment. Pesticides cause serious environmental and health problems both to humans and animals. Carbendazim (CBZ) is a broad spectrum fungicide that is used to control or effectively kill pathogenic microorganisms. CBZ is a significant contaminant found in food, soil and water. It exerts immediate and delayed harmful effects on humans, invertebrates, aquatic animals and soil microbes when used extensively and repeatedly. CBZ is a teratogenic, mutagenic and aneugenic agent that imparts its toxicity by enhancing generation of reactive oxygen species generation. It elevates the oxidation of thiols, proteins and lipids and decreases the activities of antioxidant enzymes. CBZ is cytotoxic causing hematological abnormalities, mitotic spindle deformity, inhibits mitosis and alters cell cycle events which lead to apoptosis. CBZ is known to cause endocrine-disruption, embryo toxicity, infertility, hepatic dysfunction and has been reported to be one of the leading causes of neurodegenerative disorders. CBZ is dangerous to human health, the most common side effects upon chronic exposure are thyroid gland dysfunction and oxidative hepato-nephrotoxicity. In mammals, CBZ has been shown to disrupt the antioxidant defense system. In this review, CBZ-induced toxicity in different cells, tissues and organisms, under in vitro and in vivo conditions, has been systematically discussed.

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“…[43] It has been described that hepatic damage could be observed after 4 and 12 weeks of ethanol treatment, which is evidenced by higher levels of hepatic enzyme markers and malondialdehyde. [44] For alcoholics, abnormal values for two or more of the five parameters Alanine Aminotransferase (ALAT), Aspartate Aminotransferase (ASAT), gamma-glutamyl transferase (GGT), and creatinine gave a diagnostics sensitivity of 85% and a diagnostic specificity of 64%. Likewise, elevated ALAT and ASAT levels have been described as a general indicator of tissue and organ damage caused by alcohol, viruses, infections, drugs, or toxins.…”

Section: Summary Of Key Findings and Interpretationmentioning

confidence: 99%

Effectiveness of antioxidant treatments on cytochrome P450 2E1 (CYP2E1) activity after alcohol exposure in humans and in vitro models: A systematic review

Carrasco

Souza-Mello

et al. 2021

International Journal of Food Properties

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This systematic review aimed to describe the effects of antioxidant treatments after alcohol exposure in humans and in vitro models. A systematic review of quantitative studies to identify the effectiveness of antioxidant treatments on CYP2E1 activity after alcohol consumption. Multiple databases were searched from 2010 to May 2020 for studies in English, using MeSH terms and text words relating to antioxidant treatments, CYP2E1 and, alcohol consumption. The protocol is registered on PROSPERO CRD42021226123. Study quality was assessed using the NICE methodology. The review is reported according to PRISMA. A total of eight original articles were analyzed. All papers collected and reported quantitative data. Antioxidant treatments could be beneficial after alcohol exposure to improve oxidative stress by decreasing CYP2E1 activity and increasing GSH levels. Our results suggest that antioxidant treatments could be beneficial and effective during ethanol exposure in human or in vitro models.

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Effects of Chronic Ethanol Consumption on Biochemical Parameters and Oxidative Stress on Rat

Cited by 6 publications

References 17 publications

Possiple Protective Role of Ascorbic Acid on Ethanol Induced Testicular Toxicity in Male Albino Rats

Possiple Protective Role of Ascorbic Acid on Ethanol Induced Testicular Toxicity in Male Albino Rats

Carbendazim toxicity in different cell lines and mammalian tissues

Effectiveness of antioxidant treatments on cytochrome P450 2E1 (CYP2E1) activity after alcohol exposure in humans and in vitro models: A systematic review

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