Therapeutic intervention of vitamin B12 in mitigating chronic alcoholism induced alterations in adult zebrafish (Danio rerio): a holistic in vivo approach.

BACKGROUND: Chronic alcoholism refers to the unpleasant symptoms directly resulting from excessive drinking. Increased alcohol metabolites and an unbalanced oxidative state are likely to blame for the reported effects under these circumstances. According to preclinical and clinical research, vitamin B12 can act on several organ systems with demonstrated neuroprotective, antioxidant, and glutamate modulating properties. OBJECTIVE: This research sought to examine the ameliorative effects of vitamin B12 (VtB12) in persistent alcohol (AlOH) exposed adult zebrafish with the help of following parameters like the anxiety related behavior test, Oxidative stress, and antioxidant assays, histological and immunofluorescence analysis. METHODS: Zebrafish pretreated with 0.40% AlOH (v/v) for 120 min (+AlOH) or not (-AlOH), were exposed for 6 h to home tank water (-VtB12) or to 59 µg-VtB12/kg-fish food (+VtB12) to analyze anxiety behavior in the geotaxis (novel tank) test as well as the oxidative brain damage in the adult zebrafish. RESULTS: Adult zebrafish exposed to chronic AlOH showed a decrease in the distance travelled, average and mobility speed, and increased the average frozen time, the explored area, and total no. of the site explored in the trapezoid tank. AlOH exposure also resulted in oxidative damage, enhanced lipid peroxidation, advanced oxidative protein products, decreased enzymatic and non-enzymatic antioxidant activities, and enhanced reactive oxygen species generation. Additionally, VtB12 supplementation improved neurogenesis, evident in increased Nissl cell numbers and NeuN expression in the brain. CONCLUSION: Chronic alcoholism may be effect on the brain cells as well as on the neuro-behavior of zebrafish. This research demonstrated that VtB12 shows promise as a neuroprotective agent against chronic alcoholism induced alterations in zebrafish's brain.

A systematic assessment of stress insomnia as the high-risk factor for cervical cancer and interplay of cervicovaginal microbiome.

Cervical cancer is a dreaded form of cancer in women, the fourth most common cancer, with around 0.3 million females suffering from this disease worldwide. Over the past several decades, global researches have focused on the mitigation of cervical lesions and cancers and have explored the impact of physiological and psychological stress and insomnia on cervical pathogenesis. Furthermore, disruption of the cervicovaginal microbiome profiles is identified as an added high-risk factor for the occurrence of cervical cancer. The physiological regulation of stress has an underlying mechanism controlled via hypothalamic pituitary adrenal (HPA) and sympatho-adrenal medullary (SAM) axes. Disruptions in these axes have been identified as the factors responsible for maintaining the homeostasis balance. Recent studies on microbiomes have offered novel ways to combat cervical cancer and cervix infection by exploring the interplay of the cervicovaginal microbiome. Moreover, the integration of various immune cells and microbiome diversity is known to act as an effective strategy to decipher the cervix biological activity. Cytokine profiling and the related immune competence, and physiological stress and insomnia impart to the regulatory networks underlying the mechanism which may be helpful in designing mitigation strategies. This review addressed the current progress in the research on cervical cancer, HPV infection, immune cell interaction, and physiological stress and insomnia with the cervicovaginal microbiome to decipher the disease occurrence and therapeutic management.

Long-Term Exposure of Alcohol Induced Behavioral Impairments and Oxidative Stress in the Brain Mitochondria and Synaptosomes of Adult Zebrafish.

Alcoholism causes deleterious effects such as physiological and neuronal alterations leading to the cognitive and other behavioral impairments. Mitochondrial and synaptosomal deteriorations in the brain of alcoholic persons exhibited metabolic, biochemical changes and other related risk factors, which mainly affect the brain function. This study aimed to assess the effect of chronic alcohol-induced mitochondrial and synaptosomal oxidative damage along with behavioral impairment in adult zebrafish. Zebrafish of control group received the system water and normal diet ad libitum (group I); the other groups were treated with 0.20% alcohol (group II) and 0.40% alcohol (group III) directly in fish tank for 22 days. The result revealed significant increase in lipid peroxidation, protein carbonylation, superoxide dismutase, and glutathione, and significant decline in the activity of catalase and Na+/K+ ATPase compared to control. Furthermore, the alcohol-treated zebrafish also showed significant behavioral alterations. Collectively, this regulatory mechanism demonstrates the effect of long-term alcohol consumption in the zebrafish. Our results indicate that this recreational drug "alcohol" is harmful to brain mitochondria and synaptosomes, which are the main organelles, and play an important role in memory, learning, cognitive function, and ATP formation in the brain, which may represent a significant public health concern.