EFFECT OF LONG-TERM CENTRAL BLOCKING OF HORMONE RELEASE WITH TRIPTORELIN ON OXIDATIVE STRESS MARKER ACTIVITY IN THE LIVER OF RATS

Over the past two decades, oxidative stress has been a significant concern among researchers in the field of biology worldwide. Stress can be defined as a process of altered biochemical homeostasis resulting from psychological, physiological, or environmental factors. Insufficient amounts of testosterone can worsen liver damage caused by obesity. Oxidative damage is linked to the cause of many diseases, such as cardiovascular disease, neuronal degeneration, and cancer, and also influences the aging process. The experiment was conducted on 60 sexually mature male white rats. The animals were divided into 3 groups. Group 1-control rats injected with saline (10 animals). Group 2-rats injected subcutaneously with diphereline (triptorelin) at a dose of 0.3 mg of active ingredient per kg of body weight with drug activity for 12 months (25 animals). Group 3-rats that were administered a triptorelin solution at the rate of 0.3 mg of active ingredient per kg of body weight to simulate central deprivation of luteinizing hormone synthesis with the addition of quercetin to the diet using a gastric tube based on the body weight of the animals three times a week (25 animals). Triptorelin induces oxidative damage to hepatocytes by increasing the production of reactive oxygen species and decreasing the activity of antioxidant enzymes. Oxidative damage to liver cells begins at the molecular and cellular levels as early as the 1st month of observation. Additional administration of quercetin reduces manifestations of oxidative stress by increasing the activity of antioxidant enzymes and reducing the production of reactive oxygen species.