Melatonin attenuates cardiac oxidative stress in diabetic rats following acute exhaustive exercise.

INTRODUCTION

Diabetes mellitus affects millions of people worldwide and there is evidence linking the increase of oxidative stress to the development of diabetic cardiomyopathy. Melatonin has been found to possess powerful antioxidant properties via modulating both enzymatic and non-enzymatic antioxidant systems.

OBJECTIVE

To evaluate the antioxidant potential of melatonin on the heart of diabetic animals at basal conditions and following 2 h of strenuous exercise.

METHODS

Diabetic animals were divided into two groups: non-supplemented and supplemented (melatonin). We evaluated oxidative stress biomarkers, total glutathione amount, oxidative stress index and antioxidant enzymes mRNA expression, immediately after an exhaustive exercise (IA group), and 2 h after exhausted exercise (2 h group). We also included a non-exercised group (0 h).

RESULTS

Comparing to non-exercised animals, exercise immediately induced an increase of nitrite and total antioxidant status in non-supplemented and supplemented animals, respectively. In melatonin-supplemented animals, the oxidative stress index decreased immediately after exercise (IA group) compared to non-exercised animals (0 h), an effect not seen in the non-supplemented group. Compared to non-supplemented, melatonin supplementation was shown to attenuate TBARS at all time points and increase total glutathione content at times 0 h and IA. mRNA expression of some antioxidant enzymes (CAT and GPX) was modulated by melatonin, especially when associated with exercise [catalase (CAT) and Cu, Zn superoxide dismutase (SOD)].

CONCLUSION

Our findings demonstrate that melatonin confers antioxidant protection to the diabetic heart, primarily by increasing glutathione levels and attenuating lipid peroxidation. This establishes a protective state that enhances cardiac resilience, and the combination of melatonin and exercise may offer synergistic benefits against acute, stress-induced oxidative damage in diabetic animals.