Alcohol abuse is a common phenomenon among the countries of the European continent. One of the first organs suffering from alcohol-induced damage is the liver. Activation of Kupffer cells, as part of the mononuclear phagocyte system, plays a significant role in the development of oxidative-nitrosative damage of the liver. Systemic inflammatory response affects the polarization of macrophages throughout the body and may affect the development of alcohol damage of hepatocytes. The aim of this work is to study the effect of in vivo stimulation by S. typhi bacterial lipopolysaccharide on the development of oxidative-nitrosative stress in rat liver under conditions of chronic alcohol intoxication. Male Wistar rats were randomly divided into 4 groups: I - control; II - rats received 0.4 μg/kg of bacterial lipopolysaccharide of S. typhi; III - rats with induced alcoholic hepatitis, and IV - rats with chronic alcohol intoxication and injected bacterial lipopolysaccharide. The experiment lasted 63 days. We studied pro-oxidants antioxidant enzymes, the concentration of sulfide anion, nitric oxide production and malonic dialdehyde concentration in liver tissues. In vivo administration of bacterial lipopolysaccharide enhances ethanol-induced oxidative liver damage via increased production of superoxide anion despite the adaptive increase in the activity of antioxidant enzymes. Nitric oxide, the production of which increases in the liver during prolonged stimulation of the rat body with bacterial lipopolysaccharide, chronic alcohol intoxication and their combination, mainly metabolizes to peroxynitrite

Alcohol-related liver disease is the most common cause of liver disease worldwide. The purpose of this work is the establishment of the influence of the transcription factor κB on the development of oxidative-nitrosative stress in the liver of rats under conditions of chronic alcohol intoxication. The experiments were performed on 24 male Wistar rats weighing 180-220 g. The animals were divided into 4 groups of 6 animals: control; animals, which were administered NF-κB inhibitor, namely ammonium pyrrolidinedithio­carbamate (PDTC) at a dose of 76 mg/kg 3 times a week; animals, on which we simulated alcoholic hepatitis and group of combination of alcoholic hepatitis and NF-κB inhibitor. We determined in rat liver homogenate the following biochemical parameters: the activi­ty of NO synthase isoforms, superoxide dismutase and catalase activity, the concentration of malonic dialdehyde, the concentration of peroxynitrite, nitrites and nitrosothiols, concentration of sulfide anion and superoxide anion radical production. Chronic alcohol intoxication led to increased production of reactive oxygen and nitrogen species on the background of decreased antioxidant activity, thus intensifying lipid peroxidation in the liver. Blockade of the transcription factor κB during chronic alcohol intoxication despite an increase in antioxidant activity and decrease of reactive oxygen and nitrogen species production did not ameliorate oxidative damage to the liver. Blockade of activation of nuclear transcription factor κB in rat liver by PDTC reduced the risk of oxidative damage to hepatocytes, but did not reduce the risk of developing nitrosative damage to hepatocytes. Keywords: chronic alcohol intoxication, NF-κB, oxidative-nitrosative stress, PDTC, rat liver

No abstract

Background. Dry eye disease is a multifactorial condition, which is characterized by impairment of tear film formation. Lacrimal gland metabolism plays a critical role in dry eye disease. Emotional stress may impair lacrimal gland function.Purpose. We aimed to study production of nitric oxide from constitutive and inducible NOsynthases, activity of arginases and oxidative stress markers in lacrimal glands of rats during modeling of water avoidance stress (WAS) and its correction by metformin and corvitin. Material and methods. We concluded our experiment on 36 adult male rats of Wistar line weighing 190-240 g. Animals were divided into 6 groups consisting of 6 animals each, namely: control group, WAS group, group of correction by metformin (200 mg/kg) and group of correction by corvitin (10 mg/kg) during WAS modeling. And two drug-control groups.Results. WAS leads to increased activity of inducible NO-synthase, superoxide dismutase, catalase and concentration of MDA by 1.59, 1.93, 1.97 and 1.28 times respectively. Metformin and corvitin decreased activity of inducible NO-synthase by 8.25 and 8.5 times respectively, concentration of MDA decreased by 1.35 and 1.26 times respectively. Activities of superoxide dismutase did not change after introduction of metformin and corvitin. Metformin decreased catalase activity by 1.47 and corvitin increased it by 1.55 times. Production of superoxide dropped during WAS by 1.59 times and was increased to level below or equal to that of control animals with introduction of metformin and corvitin. Conclusion. Increased activity of inducible NO-synthase during WAS is a possible reason of tissue damage in lacrimal glands of rats. Introduction of metformin or corvitin duringWAS is an effective means for correction of tissue damage in lacrimal glands of rats due to their ability to lower increased inducible NO-synthase activity.

No abstract