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Cadmium is an extremely toxic pollutant of the environment. It has many toxic effects in several organisms and its toxicity is exerted by the oxidative damages that it induces at the cellular level. Its long half-life (15 to 30 years) allows it to accumulate in many organs and tissues. Mitochondria are the main targets of cadmium. Cellular mode of action of cadmium on the functioning of the Mitochondrial Electronic Transport Chain (METC) remains unclear.
The present study is carried out to examine the mechanism of cadmium Cd-induced toxicity (500 µM) in isolated yeast mitochondria and the possible potential role of aspirin (500 µM) under (Cd2+) toxicity. We evaluated the effects of Cd on mitochondrial function such as Respiratory Electron Chain (state 3 and 4), Respiratory Control Ratio (RCR), Transmembrane Electrical Potential (∆Ψ), ATP levels, ROMs generation, Antioxidant enzyme Catalase (CAT), MalonyDialdehyde (MDA/lipid peroxidation) level and finally test the effect of aspirin on these changes. Cd affects the oxygen consumption of mitochondria respiration chain by a decrease in the rate of ADP phosphorylation (inhibition of State 3). Strong Stimulation of oxygen consumption in state 4 is observed. A decrease in (RCR) value observed is due to the disturbances observed in oxidations rates of states 3 and 4.
These results suggest that mitochondrial damage observed, resulting in the uncoupling of the oxidative phosphorylation, depression in ATP synthesis level, reduction of RCR and dissipation of transmembrane electrical potential (∆Ψ) which is the fundamental parameter of the oxidative phosphorylation via the mitochondrial complex V. We also observed an increase in antioxidant enzyme (CAT) and level of stress metabolites such as malondialdehyde (MDA), and ROMs in Cd-treated organelles. Addition of aspirin to mitochondrial suspension attenuated Cd negative effect on these parameters. Evaluation of the energetic regulation of the COx and AOX patways under Cd treatment was carried out. The results showed that Cd induced a strong inhibition of the COx pathway and the addition of aspirin seems to maintain this effect. Aspirin could form a complex with Cd, capable of generating strong resistance in yeast mitochondria to induced toxicity.