Figure 2.

Schematic of H₂S mechanism related to glutathione GSH and nuclear factor (erythroid-derived 2)-like 2 NRF2 targets in oxidative cell-damage. The endogenous release of H₂S increases GSH synthesis and blocks reactive oxygen species ROS production. When the cellular level of H₂S is increased, Kelch-like ECH-associated protein 1 Keap1 protein is S-sulfhydrated SSH: which brings a conformational change of the protein and NRF2 release from Keap1. NRF2 translocates to the nucleus, binding to the promoter containing antioxidant response element (ARE) sequences and increased transcription of antioxidant genes as catalase CAT, superoxide dismutase SOD1, glutathione-S-transferase GST, glutathione peroxidase GPx. AOE: antioxidant enzyme.