Figure 4.

Proposed pathophysiology of H₂S -induced neurotoxicity. Acute exposure to high levels of H₂S induces lung edema, leading to reduced oxygen absorption in the lungs. H₂S also affects the cardiovascular system, inducing vasodilation leading to hypotension. Together, both lead to development of ischemic hypoxia in the brain. The function of cytochrome c oxidase in the mitochondrial electron transport chain is also inhibited by H₂S, leading to reduced ATP production. Collectively, these pathophysiologic effects, coupled with direct cellular effects, account for the acute neurotoxic effects and the subsequent development of prolonged neurological sequelae.