QUERCETIN AS A MODULATOR OF OXIDATIVE DYSFUNCTIONS IN LACRIMAL GLAND TISSUES OF RATS UNDER LIPOPOLYSACCHARIDE-INDUCED SYSTEMIC INFLAMMATORY RESPONSE

The objective of this study was to investigate the effect of quercetin on the production of the primary oxidative stress effector, superoxide anion radical, in the tissues of lacrimal glands (LG) under conditions of lipopolysaccharide (LPS)-induced systemic inflammatory response (SIR). The research was conducted on 21 Wistar rats, divided into three groups: the first (control), the second (undergoing LPS-induced SIR modeling), and the third (animals receiving quercetin at a dose of 200 mg/kg via gastric gavage daily during the final week of LPS-induced SIR modeling). SIR was induced using Salmonella typhi LPS. The study has demonstrated that LPS-induced SIR significantly increased the production of superoxide anion radical in LG tissues. The activation of NADPH-dependent electron transport systems, the mitochondrial electron transport chain, and leukocyte NADPH oxidase were identified as key sources of oxidative stress under these conditions. The administration of quercetin effectively reduced the production of superoxide anion radical by all investigated sources, including NADPH-dependent enzymes, the mitochondrial electron transport chain, and leukocyte NADPH oxidase. The study enables us to conclude that quercetin can suppress oxidative stress and restore the function of lacrimal glands.