Introduction:Hydrogen sulfide (H2S), a colorless, water soluble, flammable gas with a characteristic smell of rotten eggs, has been known as a highly toxic gas for several years. However, much like carbon monoxide (CO) and nitric oxide (NO), the initial negative perception of H2S has developed with the discovery that H2S is generated enzymatically in animals under normal conditions. With the result of this discovery, much more work is needed to elucidate the biologic effects of H2S. In recent years, its cytoprotective properties have been recognized in multiple organs and tissues. In particular, H2S plays important roles in combating oxidative species such as reactive oxygen species (ROS) and reactive nitrogen species (RNS) and protect the body from oxidative stress. Therefore, this review discusses the biologic effect of H2S and how it protects cells in various diseases by acting as an antioxidant that reduces excessive amounts of ROS and RNS.Ethics and dissemination:Ethical approval and informed consent are not required, as the study will be a literature review and will not involve direct contact with patients or alterations to patient care.Conclusion:H2S has been found to be cytoprotective in oxidative stress in a wide range of physiologic and pathologic conditions, an increasing number of therapeutic potentials of H2S also have been revealed. However, there is still much debate on the clear mechanism of action of H2S, so that the mechanisms of cell signaling that promote cellular survival and organ protection need to be further investigated to provide better H2S-based therapeutics.

Autophagy is a process involving the self-digestion of components that participates in anti-oxidative stress responses and protects cells against oxidative damage. However, the role of autophagy in the anti-oxidative stress responses of melanocytes remains unclear. To investigate the role of autophagy in human epidermal melanocytes, we knocked down and overexpressed ATG7, the critical gene of autophagy, in normal human epidermal melanocytes. We demonstrated that ATG7-dependent autophagy could affect melanin content of melanocytes by regulating melanogenesis. Moreover, suppression of ATG7-dependent autophagy inhibits proliferation and promotes oxidative stress-induced apoptosis of melanocytes, whereas enhancement of ATG7-dependent autophagy protects melanocytes from oxidative stress-induced apoptosis. Meanwhile, deficiency of ATG7-dependent autophagy results in premature senescence of melanocytes under oxidative stress. Notably, we verified that ATG7-dependent autophagy could alter oxidative stress homeostasis by regulating reactive oxygen species (ROS) production, nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway, and the activity of several antioxidant enzymes in melanocytes. In conclusion, our study suggested that ATG7-dependent autophagy is indispensable for redox homeostasis and the biological functions of melanocytes, such as melanogenesis, proliferation, apoptosis, and senescence, especially under oxidative stress.