Correction of neurotoxicity and pathological changes in the salivary glands of animals in conditions of alcoholic neuropathy

Abstract

Summary. Alcohol abuse and dependence is one of the biggest public health problems in the world. Peripheral polyneuropathy is observed in approximately 46.3 % of chronic alcoholics, manifesting as a progressive, mainly sensory neuropathy. The aim of the study – to research the influence of alcoholic neuropathy on the development of pathological changes in the salivary glands of rats, as well as to substantiate the possibility of correction of the detected changes with Cocarnit. Materials and Methods. Alcoholic neuropathy was modeled by alcoholization of animals with increasing ethanol concentration for 72 days (1–24 days – 11.8 %; 25–48 – 23.6 %; 49–72 days – 37 %). The experiments were performed on 33 white nonlinear rats of both sexes weighing 180–220 g. After confirming the development of polyneuropathy on the 72nd day of the experiment, Cocarnit (World Medicine) was administered intramuscularly for 9 days at 1 mg/kg dissolved in 0.5 % lidocaine hydrochloride. In the submandibular salivary glands of rats, total proteolytic activity, total antitryptic activity, amylase activity, content of TBA-active products, content of oxidatively modified proteins and catalase activity were determined. Results. It was found that the alcoholization of rats caused an increase in the salivary glands of animals the content of TBA-active products, oxidatively modified proteins on the background of statistically unchanged catalase activity, which indicates the development of oxidative stress. Under these conditions, amylolytic activity probably decreased in the salivary glands of rats, and the proteinase-inhibitor balance did not change. Cocarnit prevents the development of neurotoxicity in rats, as evidenced by an increase in the threshold of pain sensitivity. Administration of Cocarnit for 9 days against the background of simulation of alcoholic neuropathy reliably increased the activity of amylase in the salivary glands of animals and prevented the development of carbonyl-oxidative stress, as evidenced by a significant decrease in the content of TBA-active products, oxidatively modified proteins compared to animals that were induced alcoholism without correction . Conclusions. Alcoholization of animals causes the development of alcoholic neuropathy, which leads to inhibition of amylase synthesis, causes carbonyl-oxidative stress in salivary glands of animals. Cocarnit prevents the development of neurotoxicity and suppresses carbonyl-oxidative stress in the submandibular salivary glands and restores protein synthetic function

Keywords

• alcoholic neuropathy
• cocarnit
• salivary glands
• oxidative stress
• amylase