Features of oxidative stress in alcoholism

Prokopieva, V. D.; Vetlugina, T.P.

doi:10.18097/pbmc20236902083

Cited by 3 publications

(2 citation statements)

References 69 publications

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“…There are changes in these parameters and the activity of antioxidant enzymes (SOD and catalase) in patients with AUD. Studies indicate that, at a particular stage of the disease, oxidative stress could play a protective rather than pathogenic role in the body [ 129 ]. There are also several genes related to DTs [ 130 ].…”

Section: Future Directionmentioning

confidence: 99%

Alterations in Neurotrophins in Alcohol-Addicted Patients during Alcohol Withdrawal

Malewska-Kasprzak,

Skibińska,

Dmitrzak-Węglarz

2024

Brain Sciences

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Background: Alcohol use disorder (AUD) is related to mental and somatic disorders that result in alcohol withdrawal syndrome (AWS), with 30% of AWS cases leading to life-threatening delirium tremens (DTs). Currently, studies do not support using any one biomarker in DTs. Neurotrophins affect neuromodulation, playing a role in the pathogenesis of AUD, AWS, and DTs. Methods: This review aims to summarize experimental and clinical data related to neurotrophins and S100B in neuroplasticity, as well as neurodegeneration in the context of AUD, AWS, and DTs. This work used publications that were selected based on the protocol consistent with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement. Results: The BDNF level could be a good candidate biomarker for relapse susceptibility, as it is significantly reduced during consumption and gradually increases during abstinence. GDNF influences AUD through its integral role in the function of dopaminergic neurons and ablates the return to alcohol-drinking behavior. NGF protects neurons from ethanol-induced cytotoxic damage and affects recovery from cognitive deficits after brain damage. The NT-3 level is decreased after alcohol exposure and is involved in compensatory mechanisms for cognitive decline in AUD. NT-4 affects oxidative stress, which is associated with chronic alcohol consumption. S100B is used as a biomarker of brain damage, with elevated levels in serum in AUD, and can protect 5-HT neurons from the damage caused by alcohol. Conclusions: BDNF, GDNF, NT-3, NT-4, NGF, and S100B may be valuable markers for withdrawal syndrome. In particular, the most relevant is their association with the development of delirium complications. However, there are few data concerning some neurotrophins in AWS and DTs, suggesting the need for further research.

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Section: Future Directionmentioning

confidence: 99%

Alterations in Neurotrophins in Alcohol-Addicted Patients during Alcohol Withdrawal

Malewska-Kasprzak,

Skibińska,

Dmitrzak-Węglarz

2024

Brain Sciences

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“…Studies have shown that alcohol can interfere with the function of the hypothalamus-pituitary-gonadal (HPG) axis and reduce the production of gonadotropin releasing hormone (GnRH), luteinizing hormone, and follicle-stimulating hormone, resulting in the impairment of the activity of Leydig and Sertoli testicular cells, which play a crucial role in testosterone production and sperm maturation respectively [7]. Moreover, alcohol metabolism generates an excess of reactive oxygen species (ROS), thereby causing a discrepancy in the oxi-dative stress status of the organism [8,9]. This mechanism is considered the main way by which alcohol induces ultrastructural changes in the male reproductive system.…”

Section: Introductionmentioning

confidence: 99%

Phycocyanin alleviates alcohol-induced testicular injury in male Wistar rats

Boukari,

Ghoghbane,

Khemissi

et al. 2024

Clin Exp Reprod Med

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Objective: Given the noteworthy implications of alcohol consumption and its association with male infertility, there has been a notable focus on investigating natural alternatives to mitigate its adverse effects. Thus, this study was conducted to assess the potential protective effect of phycocyanin extract derived from the blue algae Arthrospira (Spirulina) platensis against ethanol-induced oxidative stress, disturbances in testicular morphology, and alterations in sperm production.Methods: Male rats were divided into four groups (five rats each): the control group received a saline solution, the ethanol exposed group (EtOH) was subjected to intraperitoneal injections of 10 mL/kg of ethanol solution at a concentration of 38% (v/v), the phycocyanin alone treated group (P) received oral administration of phycocyanin at a dosage of 50 mg/kg, and the phycocyanin-cotreated group (PE) was given oral phycocyanin followed by ethanol injections. All treatments were administered over a period of 14 days.Results: Our findings demonstrated that ethanol exposure induced reproductive toxicity, characterized by reduced sperm production and viability, alterations in testicular weight and morphology, increased lipid peroxidation levels, and elevated oxidative enzyme activity. In addition, the ethanol-intoxicated group showed perturbations in serum biochemical parameters. However, the simultaneous exposure to ethanol and phycocyanin exhibited a counteractive effect against ethanol toxicity.Conclusion: The results showed that supplementation of phycocyanin prevented oxidative and testicular morphological damage-induced by ethanol and maintained normal sperm production, and viability.

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