Recently, the possible involvement of H 2S in demyelinating disorders and nerve degenerative disorders has also been suggested. The regeneration of these injured peripheral nerves is associated with the demyelination, dedifferentiation, and proliferation of Schwann cells, which takes place serially. Additionally, following injury in the peripheral nervous system (PNS), peripheral nerves undergo Wallerian degeneration and macrophages are recruited into the distal nerve pump. The neuromodulation and neuroprotection of nerve cells are a common feature of H 2S and its enzymes exert effects in a variety of diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Down’s syndrome, cerebral ischemia, and Huntington’s disease. Īlthough it is known that H 2S protects nerves from oxidative stress, saves photoreceptor cells in the retina from light-induced degeneration, regulates endoplasmic reticulum stress, and defends the kidneys from ischemic reperfusion injury, the role of H 2S in the central nervous system (CNS) has attracted a lot of attention over the past few decades. Various studies performed on rat, human, and bovine brain tissues have determined that H 2S is present at levels of up to 50–160 μmol/L in tissues and that sodium hydrogen sulfide (NaHS) is one of the physiological donors of H 2S. The high lipid solubility of H 2S allows it to easily penetrate the plasma membrane of cells in its undissociated form but it remains unclear whether this undissociated form is physiologically pertinent.
At a pH of 7.4 in the mammalian body, one-fifth of the total H 2S subsists in an undissociated form, with the remaining content existing as hydrosulfide anions (HS −) and sulfide (S 2−). H 2S is a sulfur analog of water and, due to its weak intermolecular force, exists in a gaseous form that is colorless but has an offensive odor. Furthermore, a reevaluation of the endogenous levels of H 2S confirmed its existence and advantages in mammalian tissues. However, in recent years, the benefits of gasotransmitters such as nitric oxide (NO) and carbon monoxide (CO) have acted as a fillip to investigating the benefits of H 2S. As a result, the beneficial roles of this compound were neglected for many years due to its toxic nature. It acts as a gaseous signaling molecule and chemical reagent involved in many physiological processes, including the pathogeneses of various diseases such as neurodegenerative disease, heart failure, and diabetes. Hydrogen sulfide (H 2S) is a poisonous gas that is a toxicant in most organs in the human body. The primary purpose of this review was to provide an overview of the role of H 2S in the human body and to describe its beneficial effects.
To date, physiological and toxic levels of H 2S in the human body remain unclear and most of the mechanisms of action underlying the effects of H 2S have yet to be fully elucidated. Previous studies have shown that H 2S plays important roles in peripheral nerve regeneration and degeneration and has significant value during Schwann cell dedifferentiation and proliferation but it is also associated with axonal degradation and the remyelination of Schwann cells. H 2S exerts a wide range of pathological and physiological functions in the human body, from endocrine system and cellular longevity to hepatic protection and kidney function. It is produced by the enzymes cystathionine β-synthase (CBS), cystathionine ϒ-lyase (CSE), 3-mercaptopyruvate sulfurtransferase (MST), and D-amino acid oxidase (DAO), which are also involved in tissue-specific biochemical pathways for H 2S production in the human body. H 2S exerts universal cytoprotective effects and acts as a defense mechanism in organisms ranging from bacteria to mammals.
Hydrogen sulfide (H 2S) is an emerging neuromodulator that is considered to be a gasotransmitter similar to nitrogen oxide (NO) and carbon monoxide (CO).
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