The effect of hyperoside on superoxide dismutase (SOD) activity in mice brain and liver

Background. Superoxide dismutase is a key antioxidant enzyme that protects cells by converting harmful superoxide radicals into hydrogen peroxide and oxygen. Research indicates that hyperoside exhibits antioxidant effects by scavenging reactive oxygen species (ROS) and enhancing antioxidant enzyme activity. It has been shown to protect against hydrogen peroxide (H2O2) — induced cell damage by inhibiting apoptosis [1]. Aim. The aim of the current study was to evaluate the effect of hyperoside on the SOD activity in mice liver and brain after aluminium consumption. Methods. Experiments were conducted on 4–6 weeks old mice (20–25 g), n = 8. Mice were divided into four groups: control, hyperoside-treated, aluminum-treated, and aluminum-hyperoside-treated. Aluminum (Al³+ ) was injected into the abdominal cavity. SOD activity was determined spectrophotometrically. Results were expressed as the mean ± SD. Results. It was found that hyperoside, aluminum, and their combination significantly affected SOD activity in the liver (p < 0.05), with both aluminum and hyperoside increasing activity. However, administering hyperoside after aluminum-induced oxidative stress showed no significant difference compared to aluminum alone, despite further increasing SOD activity. In the brain, aluminum had no significant effect on SOD activity (p > 0.05), and hyperoside (50 mg/kg for 21 days) slightly reduced activity without significance. Conclusion. Despite the antioxidant properties of hyperoside, the results show that its 50 mg/kg dose does not significantly affect SOD activity in the mice brain. Meanwhile hyperoside increased SOD activity in mice liver, but it was not significantly, so its effectiveness may depend on dose, timing, warranting further research.