Search

In this study, calcium phosphate nanoparticles-based (STCNV) and montanide oil adjuvant vaccine (STOAV) containing outer membrane proteins (Omps) of S. Typhi were evaluated for inducing oxidative stress indicators [reduced glutathione (GSH), lipid peroxidation (LPO), catalase, superoxide dismutase (SOD), and total protein] in the tissues of mice after vaccination. The GSH levels though slightly high in the liver, kidney, and lungs of STCNV group were not significantly different from STOAV and the control group (STC). There was no significant difference in LPO levels in any group for any tissue. The significantly lower activities of catalase were observed in the kidney and lungs of the STCNV group as compared to STOAV and STC group, while in the liver, STCNV group revealed lower catalase activity in comparison to the control group. No significant difference in the SOD activities between the two vaccinated groups was observed. The total protein contents in all the organs showed no significant difference in the vaccinated and the control group. The vaccines may induce long-term inflammatory response and consequently damage vital organs; this study revealed no long-term oxidative stress in all the three vital organs, suggesting that these vaccines may not cause oxidative damages in the vital organs of mice. [ABSTRACT FROM AUTHOR]

Introduction: Ischemia–reperfusion injury (IRI) is the inexplicable aggravation of cellular dysfunction that results in blood flow restoration to previously ischemic tissues. COX mediates the oxidative conversion of AA to various prostaglandins and thromboxanes, which are involved in various physiological and pathological processes. In the pathophysiology of I/R injuries, COX has been found to play an important role. I/R injuries affect most vital organs and are characterized by inflammation, oxidative stress, cell death, and apoptosis, leading to morbidity and mortality. Materials and methods: A systematic literature review of Bentham, Scopus, PubMed, Medline, and EMBASE (Elsevier) databases was carried out to understand the Nature and mechanistic interventions of the Cyclooxygenase modulations in ischemic injury. Here, we have discussed the COX Physiology and downstream signalling pathways modulated by COX, e.g., Camp Pathway, Peroxisome Proliferator-Activated Receptor Activity, NF-kB Signalling, PI3K/Akt Signalling in ischemic injury. Conclusion: This review will discuss the various COX types, specifically COX-1 and COX-2, which are involved in developing I/R injury in organs such as the brain, spinal cord, heart, kidney, liver, and intestine. [ABSTRACT FROM AUTHOR]

The present study evaluated the effect of coenzyme Q10 nanoparticles (CoQ NPs) against monocrotophos (MCP) exposure-induced oxidative stress in kidney tissue of rats. Albino wistar rats were divided into four groups i.e. control, CoQ NPs-treated, MCP-treated and MCP + CoQ NPs-treated groups. An acute dose of MCP (4.5 mg/kg b.wt) dissolved in corn oil was administered while CoQ NPs were given at a dose of 100 mg/kg b.wt 2 h before MCP treatment. Results showed that MCP exposure resulted in oxidative stress generation in kidney tissue of rats as depicted by increased lipid peroxidation and protein oxidation followed by decreased glutathione content in tissue homogenate. The activity of superoxide dismutase also decreased significantly in kidney tissue. Histopathological analysis showed many cellular alterations in the kidney tissue supporting the toxic effects of MCP exposure in rats. Co-treatment of CoQ NPs with MCP significantly ameliorated the oxidative stress generation and improved the histological alterations. The results indicate that CoQ NPs have the potential to reverse the oxidative stress generated after MCP exposure in rat kidneys suggesting their therapeutic potential. [ABSTRACT FROM AUTHOR]