The Inhibitory Effect of Captopril on Paraquat Toxicity in Mitochondria Isolated from the Rat Liver

Abstract: Background: The aim of the present study was to show the capability of captopril as a thiol ACEi (angiotensin converting enzyme inhibitor),in suppressing mitochondrial toxicity due to paraquat. Method: In this study, rats liver mitochondria were isolated with buffer using refrigerated centrifuge. In order to obtain the minimum toxic dose of paraquat and the effective dose of captopril, different concentrations of paraquat (1 to 100mM)and captopril (0.08 to 1mM)were investigated by determining LC50 , viability indices, lipid peroxidation, mitochondrial swelling, catalase activity, GSH and GSSG. Results: Simultaneous treatment of mitochondria with captopril (0.08mM) and paraquat (5mM) significantly ameliorate the mitochondrial toxicity of paraquat (5mM) alone. Our results show that captopril is a effective antioxidant. The antioxidative action of captopril appears to be attributable to the sulphahydryl group (SH) in the compound. This effect may be due to captopril abilities to scavenge reactive oxygen species. Conclusion: Our results indicate that Captopril can ameliorate oxidative stress induced by paraquat and therefore, can be used for the prevention and treatment of diseases caused by environmental toxins. Keywords: Paraquat, Rat liver Mitochondria, Captopril, Oxidative stres

α-Melanocyte-Stimulating Hormone Triggers Melanogenesis Via Activation of the Aryl Hydrocarbon Receptor Pathway in B16F10 Mouse Melanoma Cells

Melanin is a group of natural pigments that determines the human skin color and provides fundamental protection against the harmful impacts of physical and chemical stimuli. The aim of this study was to establish the regulatory role of aryl hydrocarbon receptor (AhR) in α-melanocyte-stimulating hormone (α-MSH) induced melanogenesis. In the present study, following knockdown of AhR, murine B16F10 cells were treated with α-MSH (200 nM) and tyrosinase activities, cellular melanin content, mRNA levels of several important genes involved in melanogenesis including AhR, CTNNB1, TYR2, and microphthalmia-associated transcription factor (MITF) were measured as endpoints. Exposure to α-MSH led to elevated expression of AhR, CTNNB1, MITF, and TYR in accordance with increased tyrosinase enzyme activity as well as a significant rise in the total melanin content. Our results suggest that AhR plays a regulatory role in α-MSH-stimulated melanogenesis. © The Author(s) 2021