Heat stress prevents the decrease in succinate dehydrogenase activity in the extensor digitorum longus of...

Area of Science:

• Physiology
• Biochemistry
• Endocrinology

Background:

• Diabetes mellitus (DM) is associated with decreased mitochondrial function and increased oxidative stress in skeletal muscle.
• Succinate dehydrogenase (SDH) activity, heat shock protein 60 (HSP60), and superoxide dismutase 2 (SOD2) are key indicators of mitochondrial health and cellular protection.

Purpose of the Study:

• To investigate the effects of heat stress (HS) on SDH activity, HSP60, and SOD2 content in the extensor digitorum longus muscle of streptozotocin (STZ)-induced diabetic rats.
• To determine if HS can mitigate the negative impacts of diabetes on mitochondrial enzymes and antioxidant proteins.

Main Methods:

• Male Wistar rats were divided into four groups: control, HS, diabetes mellitus (DM), and DM+HS.
• Diabetes was induced using streptozotocin (STZ).
• Heat stress was applied at 42 °C for 30 minutes, 5 times a week for 3 weeks.

Main Results:

• SDH activity decreased in both DM and DM+HS groups, but was higher in the DM+HS group compared to the DM group.
• HSP60 content, reduced in the DM group, was maintained in the DM+HS group.
• SOD2 content decreased only in the DM group, suggesting HS may preserve antioxidant capacity.

Conclusions:

• Heat stress appears to prevent the decrease in SDH activity in skeletal muscle caused by diabetes.
• HS may protect against diabetes-induced mitochondrial dysfunction by maintaining SOD2 and HSP60 levels.
• These findings suggest HS could be a potential strategy to combat oxidative stress in diabetic conditions.