All aspects of the toxic effects of lipopolysaccharide on rat liver and the protective effect of vitamin E and sodium selenite

Abstract

This work was planned to research the effects of lipopolysaccharide (LPS) and/or vitamin E (VE) and sodium selenite (SS), which have antioxidant properties, administered to the liver tissue of male rats. For this purpose, histopathology, immunohistochemistry, antioxidant capacity, terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling assay, liver function, and DNA structure tests were performed. The lipid profile was also evaluated in this study. Rats that were administered LPS were treated with VE and/or SS. The liver function tests and lipid profile parameters showed statistically significant changes and histological alterations in the LPS treated groups. The number of cells entering apoptosis was increased by LPS administration when compared to the control group. LPS treatment increased the DNA damage and decreased the ferric reducing antioxidant power and trolox equivalent antioxidant capacity values when compared to the control group. VE and/or SS provided protective effects against the examined parameters. These results indicated that we can assume that the treatment of VE and SS together may be more efficient than using them individually against LPS.

Red Palm Oil Ameliorates Oxidative Challenge and Inflammatory Responses Associated with Lipopolysaccharide-Induced Hepatic Injury by Modulating NF-κβ and Nrf2/GCL/HO-1 Signaling Pathways in Rats

“…We had previously reported a decrease in some hepatic injury markers including ALT, AST and LDH in the serum of tert-butyl hydroperoxide-induced rats pre-treated with RPO [ 19 ]. Other reports have demonstrated the ability of vitamin E, β-carotene and lycopene, all important constituents of RPO to ameliorate LPS- and other chemicals-induced hepatotoxicity in rodent models [ 46 , 49 , 50 , 51 ]. We can ascribe the ability of RPO to lower elevated liver function enzymes and resolve hepatic morphological disruptions observed in our study to the stabilizing effect of RPO and/or its bioactive components on hepatocytes plasma membrane.…”

Anti-ulcerogenic effect of osajin on indomethacin-induced gastric damage in rats

“…In recent studies, reactive oxygen species (ROS) have been shown to be an important factor in the pathophysiology of GI ulcers (Atalay et al 2015;Bozkurt et al 2017), inducing oxidative stress in cells (Pandır et al 2019). It has been reported that the ROS generate oxidized products via attacking the phospholipids of the cell membrane.…”

“…The NSAIDs produce their curative effects via the inhibition on COX (cyclooxygenase) enzyme activity in cells. However, the inhibition of the COX system, which is related to arachidonic acid, causes reduced prostaglandin E 2 (PGE 2 ) synthesis that is part of the GI protective system (Rainsford 1988).In recent studies, reactive oxygen species (ROS) have been shown to be an important factor in the pathophysiology of GI ulcers (Atalay et al 2015;Bozkurt et al 2017), inducing oxidative stress in cells (Pandır et al 2019). It has been reported that the ROS generate oxidized products via attacking the phospholipids of the cell membrane.…”