Figure 1.

Heat load induces oxidative stress and mitochondrial dysfunction. Acute heat stress suppresses the activity of mitochondrial respiratory complexes I, III, and IV, downregulates uncoupling protein expression, and increases electron leakage, which in turn, leads to increased ROS production (Red arrows). Excessive ROS (O₂⁻, OH) production causes damage to the protein, lipid, and DNA. Chronic heat stress, on the other hand, reduces the metabolic capacity of mitochondria via downregulating the activity and expression of antioxidant enzymes, and depleting the body’s antioxidant reserves, which causes accumulation of ROS—breaking the oxidative balance and inducing oxidative stress (yellow arrows).