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A study was conducted to investigate the potential protective effects of Bacopa monnieri extract on alcohol-induced toxicity in rats, focusing on its hypolipidemic and cardioprotective properties. For a period of 30 days, the experimental rats were orally intoxicated with alcohol (2 g/kg body weight) daily. Simultaneously, Bacopa monnieri extract was administered at a dose of 200 mg/kg body weight. The results of the study revealed that the rats subjected to alcohol-induced toxicity experienced a significant reduction in antioxidant defense systems, such as reduced glutathione (GSH) and ascorbic acid, while the activity of glutathione-S-transferase was enhanced compared to the control group. Additionally, the alcoholinduced group exhibited increased levels of triglycerides (TG) and total cholesterol (TC), as well as a significant decrease in phospholipids (PL). However, when Bacopa monnieri was supplemented along with alcohol, it significantly improved the antioxidant status and normalized the lipid profiles. These findings suggest that Bacopa monnieri possesses cardioprotective and hypolipidemic activities, which provide protection against alcohol-induced toxicity [ABSTRACT FROM AUTHOR]

Objective Alcoholism arises from combined effects of multiple biological factors including genetic and non-genetic causes with gene/environmental interaction. Intensive research and advanced genetic technology has generated a long list of genes and biomarkers involved in alcoholism neuropathology. These markers reflect complex overlapping and competing effects of possibly hundreds of genes which impact brain structure, function, biochemical alcohol processing, sensitivity and risk for dependence. Method We compiled a tabular list of clinically relevant genetic biomarkers for alcoholism targeting expression disturbances in the human brain through an extensive search of keywords related to alcoholism, alcohol abuse, and genetics from peer reviewed medical research articles and related nationally sponsored websites. Gene symbols were then placed on high resolution human chromosome ideograms with gene descriptions in tabular form. Results We identified 337 clinically relevant genetic biomarkers and candidate genes for alcoholism and alcohol-responsiveness from human brain research. Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2 , MAOA , and COMT ), serotoninergic (e.g., HTR3A , HTR1B , HTR3B , and SLC6A4 ), GABAergic (e.g., GABRA1 , GABRA2 , and GABRG1 ), glutaminergic ( GAD1 , GRIK3 , and GRIN2C ) and opioid (e.g., OPRM1 , OPRD1 , and OPRK1 ) pathways which presumably impact reinforcing properties of alcohol. Gene level disturbances in cellular and molecular networks impacted by alcohol and alcoholism pathology include transketolase (TKT), transferrin (TF), and myelin (e.g., MBP, MOBP, and MOG). Conclusions High resolution chromosome ideograms provide investigators, physicians, geneticists and counselors a convenient visual image of the distribution of alcoholism genetic biomarkers from brain research with alphabetical listing of genes in tabular form allowing comparison between alcoholism-related phenotypes, and clinically-relevant alcoholism gene(s) at the chromosome band level to guide research, diagnosis, and treatment. Chromosome ideograms may facilitate gene-based personalized counseling of alcohol dependent individuals and their families. [ABSTRACT FROM AUTHOR]

Chronic alcohol use alters adaptive immunity and cytokine activity influencing immunological and hormone responses, inflammation, and wound healing. Brain cytokine disturbances may impact neurological function, mood, cognition and traits related to alcoholism including impulsiveness. We examined the relationship between plasma cytokine levels and self-rated psychiatric symptoms in 40 adult males (mean age 51 ± 6 years; range 33-58 years) with current alcohol dependence and 30 control males (mean age 48 ± 6 years; range 40-58 years) with no history of alcoholism using multiplex sandwich immunoassays with the Luminex magnetic-bead based platform. Log-transformed cytokine levels were analyzed for their relationship with the Symptom Checklist-90R (SCL-90R), Barratt Impulsivity Scales (BIS) and Alcoholism Severity Scale (ASS). Inflammatory cytokines (interferon γ-induced protein-10 (IP-10); monocyte chemoattractant protein-1 (MCP1); regulated on activation, normal T cell expressed and secreted (RANTES)) were significantly elevated in alcoholism compared to controls while bone marrow-derived hematopoietic cytokines and chemokines (granulocyte-colony stimulating factor (GCSF); soluble CD40 ligand (sCD40L); growth-related oncogene (GRO)) were significantly reduced. GRO and RANTES levels were positively correlated with BIS scales; and macrophage-derived chemokine (MDC) levels were positively correlated with SCL-90R scale scores (p < 0.05). Elevated inflammatory mediators in alcoholism may influence brain function leading to increased impulsiveness and/or phobia. The novel association between RANTES and GRO and impulsivity phenotype in alcoholism should be further investigated in alcoholism and psychiatric conditions with core impulsivity and anxiety phenotypes lending support for therapeutic intervention. [ABSTRACT FROM AUTHOR]

The total antioxidant activity (TAA) of human serum blood of patients suffering from alcoholism was tested by cathode voltammetry with a model process of oxygen electroreduction. A known spectrophotometrical method was used for comparison. As results the total antioxidant activity of serum blood of patients with alcoholism was estimated by voltammetry during therapy in hospital. It was shown the TAA of serum blood of patients in pathology before and after treatment is lower than that one of healthy people. However, during the process of 10 days of alcoholism treatment the TAA coefficient increases. The relationship between the coefficient of total antioxidant activity of human serum blood and the stage of treatment was detected. [ABSTRACT FROM AUTHOR]

No abstract available for this article. [ABSTRACT FROM PUBLISHER]

Despite reduced levels of noradrenaline and increased cortical β-adrenergic receptor binding, there is controversy regarding the effect of chronic alcohol consumption on the noradrenergic neurons of the locus coeruleus (LC). The aim of this study is to investigate the effects of chronic alcohol consumption on the LC; in particular, to determine whether or not there is any alteration in the size or number of neurons, or other significant changes in this nucleus. Eight chronic alcoholics without additional medical complications and eight age-matched controls were selected for this study. Immunohistochemis-try with antibodies against tyrosine hydroxylase (TH) was used to visualize TH-positive neurons in spaced serial 50-μm sections throughout the length of the LC. These neurons were counted and no correction factors applied. There was no significant loss of TH-positive neurons in the LC of alcoholics compared with controls who had up to 20% variation in the number of neurons between individuals. This confirms published results from one alcoholic without complications, but contradicts recent findings of a significant neuronal loss in five alcoholics, all with liver pathology. Our analysis suggests that central noradrenergic neurons in alcoholics without significant medical complications are not susceptible to alcohol neurotoxicity. [ABSTRACT FROM AUTHOR]

The development of alcohol dependence is a complex process influenced by both genetic and environmental risk factors (Prescott and Kendler 1999). The relative contributions of genetic and environmental influences fluctuate [...]