PROTECTIVE EFFECT OF L-CARNITINE AND BAKER YEAST SACCHAROMYCES CEREVISIAE AGAINST HEPATIC TOXICITY INDUCED BY VALPROATE AS ANTIEPILEPTIC DRUG IN RATS

Objective: The aim of this work was to investigate the protective role of L-carnitine and baker yeast (Saccharomyces cerevisiae) against the effect of sodium valproate (VPA) induced toxicity and oxidative stress in the liver.Methods: Chronic administration of sodium valproate was studied by oral administration of VPA for six months. The protective effect was conducted by an administration of L-carnitine or/and baker yeast for one month before chronic administration of VPA. Some biochemical parameters, lipid profile, oxidative stress and histopathological studies were analyzed.Results: Chronic administration of VPA for six months caused a significant increase in serum amino transferases (AST, ALT), alkaline phosphatase (ALP), bilirubin, total lipids, total cholesterol, low density lipoprotein (LDL) as well as oxidative stress; malodialdehyde (MDA) and nitric oxide. While decreased total protein, albumin, and globulin in addition to glutathione peroxidase and superoxide dismutase (SOD). The administration of L-carnitine and baker yeast cause significant decreases in the activities of AST, ALT, bilirubin, lipid peroxidation, LDL level and MDA levels and return the levels of total protein, albumin, globulin, glutathione peroxidase and SOD to the normal levels. Histopathological results revealed improvement of the liver structure.Conclusion: L-carnitine and baker yeast (Saccharomyces cerevisiae) offer protection to the liver by preserving the structural integrity of hepatocellular membrane against sodium valproate induced hepatotoxicity and oxidative stress.Â

The Effects of Gamma Irradiation on the Optical and Electrical Properties of Melt Quench Ge18Bi4Se78 Chalcogenide Glass.

The structural, optical, and electrical properties of as-deposited and gamma irradiated (50, 100, 150kGy) Ge18Bi4Se78 thin films have been investigated. The structural characteristics of both the as-deposited and gamma irradiated films are inspected by X-ray diffraction (XRD).The optical constants of all the films are analyzed in the wavelength range 250-2500 nm employing spectrophotometer measurements at normal incidence. The type of transition is estimated using the obtained optical constants. The optical energy gap Eop as well as Urbach Eu energy in addition to plasma frequency ωp are studied. Single oscillator and Drude models are used to discuss the refractive index in the normal dispersion region. The effect of γ irradiation on the DC conductivity of the considered films is inspected

Association of interleukin-6 polymorphisms with obesity or metabolic traits in young Mexican-Americans

Objective The objective of the study is to investigate the association of interleukin-6 (IL6) promoter single-nucleotide polymorphisms rs1800797 (-597 G/A) and rs1800796 (-572 G/C) with obesity or metabolic syndrome in Mexican-Americans. Methods The rs1800797 and rs1800796 single-nucleotide polymorphisms were genotyped in Mexican-Americans (n = 437) from South Texas, and results were correlated with measures of obesity and metabolic syndrome including body mass index, waist circumference, blood pressure, cholesterol, triglycerides, glucose, liver enzymes, plasma IL6 and high-sensitive C-reactive protein (hs-CRP). Results Significant associations were found for the rs1800796 variant with increased waist circumference, insulin resistance, lower IL6 levels and higher hs-CRP levels. The rs1800797 variant showed no associations with metabolic traits but was associated with higher IL6 levels and lower hs-CRP levels. Conclusions Findings in this study support the anti-inflammatory, anti-obesity and glucose homeostatic roles of IL6 in Mexican-American youth

DNA damage in obesity: Initiator, promoter and predictor of cancer

Epidemiological evidence linking obesity with increased risk of cancer is steadily growing, although the causative aspects underpinning this association are only partially understood. Obesity leads to a physiological imbalance in the regulation of adipose tissue and its normal functioning, resulting in hyperglycaemia, dyslipidaemia and inflammation. These states promote the generation of oxidative stress, which is exacerbated in obesity by a decline in anti-oxidant defence systems. Oxidative stress can have a marked impact on DNA, producing mutagenic lesions that could prove carcinogenic. Here we review the current evidence for genomic instability, sustained DNA damage and accelerated genome ageing in obesity. We explore the notion of genotoxicity, ensuing from systemic oxidative stress, as a key oncogenic factor in obesity. Finally, we advocate for early, pre-malignant assessment of genome integrity and stability to inform surveillance strategies and interventions