PROFILING OF MITOCHONDRIAL ENZYMES IN AT2 ADMINISTRATION AND HESPERIDIN

The mitochondrial enzyme profile is essential in maintaining cellular bioenergetics, especially in oxidative stress and metabolic disorders. This study evaluates the effects of angiotensin II (AT2) administration on mitochondrial function and the potential protective effects of Hesperidin. A total of 30 wistar rats weighing between 120-170 mg/kg were used for this experiment. The animals were allowed to acclimatize for 4 weeks and they were selected randomly into 6 different groups with 6 rats in each group described as follows; Group 1: Control, rats were given feed and water only; Group 2: Angiotensin II, rats were given angiotensin II only (0.001 ml/kg); Group 3: Angiotensin II + Telmisartan, rats were given Angiotensin II (0.001 ml/kg) + Telmisartan (0.002 ml/kg); Group 4: Angiotensin II + Hesperidin, rats were given Angiotensin II (0.001 ml/kg) + Hesperidin (0.001 ml/kg); Group 5: Telmisartan, rat were given Telmisartan only (0.002 ml/kg), and Group 6: Hesperidin, rats were given Hesperidin (0.001 ml/kg). At the end of the 4-week experimental period, the rats were subjected to an overnight fast and anaesthetized. The anaesthetized animals were bled by cardiac puncture and liver tissue was harvested and homogenized. The whole blood was collected, allowed to be clotted and then centrifuged. The results revealed hesperidin and Telmisartan were significantly higher compared to the Control group whereas Angiotensin II were significantly higher than Angiotensin II + Telmisartan and Angiotensin + Hesperidin. The histological examination showed normal liver histology with the hepatocytes appearing normal while central vein appeared enlarged. In conclusion, Telmisartan and Hesperidin both act to reduce NADH reductase activity and improve mitochondrial function and reduce mitigating oxidative stress and inflammation. Hesperidin alone showed a significant reduction in NADH reductase activity, The results underscore the importance of addressing oxidative stress and mitochondrial dysfunction in managing conditions associated with elevated Angiotensin II, such as hypertension and cardiovascular disease.