Diallyl Trisulfide Prospectively Retrieves Arsenic Induced Lung Oxidative Stress, Inflammation Through the Activation of Nrf2/HO-1 Signaling

Abstract

Background: Arsenic (As), an entrenched natural cancer-causing agent, has been found to cause oxidative pressure initiated fiery lung maladies in people upon unending introduction. The aim of our examination is to explore the ameliorative capability of garlic polysulfide, i.e., diallyl trisulfide (DATS), against As-initiated oxidative lung damage in rodents. Methods: Rats were directed with As (5 mg/kg BW) for about a month and treated as lethal control. The treatment convention was made by the pre-administration of DATS (40 mg/kg BW, PO) for about a month in As-treated rodents. Prooxidant and antioxidant status, oxidative markers, and Nrf2 and its related ARE and tissue morphometric investigations were performed in the lungs of rodents. Results: As inebriation essentially expanded the dimensions of free radicals, inflammatory cytokines, and lung edema (wet to dry weight proportion) when contrasted with control rodents. Moreover, lung oxidative pressure markers, for example, malonaldehyde (MDA) and myeloperoxidase (MPO), were likewise altogether expanded in As-treated rats. Histological and immunohistochemical (iNOS) analyses additionally uncovered that the As initiated provocative changes in the lung tissue of rodents. Pre-administration of DATS essentially improved the cell reinforcement status and restrained the oxidative pressure, cytokines, and Keap1 protein by means of the actuation of Nrf2 translocation into the nucleus. Conclusion: Morphometric, biochemical, histological, and immunohistochemical examination remarkably exhibited that DATS was proficient in limiting the fiery harm in lung tissue and improved the oxidative pressure. By and large, our outcomes prescribe that DATS may be a potential remedial contender for treating oxidative and inflammatory lung damage and hence warrants additionally examination.