In rats, a single dose of kisspeptin-10 given after a brain injury caused by excess methionine helped protect brain cells. It lowered markers of oxidative damage, boosted the brain's natural antioxidant glutathione, and restored the activity of an important antioxidant enzyme (SOD). The peptide itself didn’t cause any extra cell death.

Apart from its effect on the regulation of reproductive function, recent studies indicate that kisspeptin may play roles in the antioxidant defense system. The antioxidant defense system and oxidative stress contribute to the etiology and pathogenesis of neuronal cell death after brain injury. We have investigated the postacute effect of kisspeptin-10 on brain injury induced by L-methionine. DNA fragmentation, malondialdehyde (MDA), reduced glutathione levels, and superoxide dismutase (SOD) activities were analyzed. Our results showed that methionine treatment increases apoptotic cell death. Kisspeptin alone showed no side effect on apoptotic cell death. However, kisspeptin treatment reversed the proapoptotic effect of methionine associated with reduced MDA and increased glutathione levels. Furthermore, SOD activity was completely depleted in methionine-treated animals. In conclusion, our results revealed that delayed kisspeptin-10 treatment reduces neuronal cell death by activation of SOD activity.