This study examined the important relationship between cystathionine γ-lyase (CSE) functionality and cysteine supply for normal growth and life span. Mice with a targeted deletion of the CSE gene (CSE-KO) were fed a cysteine-limited diet and their growth and survival patterns as well as levels of cysteine, homocysteine, glutathione, and hydrogen sulfide (H2S) were measured. CSE-KO mice fed a cysteine-limited diet exhibited growth retardation; decreased levels of cysteine, glutathione, and H2S; and increased plasma homocysteine level. However, histological examinations of liver did not reveal any abnormality and plasma levels of aspartate aminotransferase, alanine aminotransferase, and albumin were normal in these animals. No CSE-KO mice survived after 12 weeks of feeding with the cysteine-limited diet. Supplementation of H2S to the CSE-KO mice failed to reverse the aforementioned abnormalities. On the other hand, supplementation of cysteine in the drinking water of the CSE-KO mice significantly increased plasma cysteine and glutathione levels. This eventually led to an increase in body weight and rescued the animals from death. In conclusion, CSE is critical for cysteine biosynthesis through the transsulfuration pathway and the combination of CSE deficiency and lack of dietary cysteine supply would threaten life sustainability.
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http://dx.doi.org/10.1016/j.freeradbiomed.2011.01.038 | DOI Listing |
Nitric Oxide
October 2024
School of Natural Sciences, Laurentian University, Sudbury, Canada; Cardiovascular and Metabolic Research Unit, Laurentian University, Sudbury, Canada. Electronic address:
Cystathionine gamma-lyase (CSE) is a key enzyme in reverse transsulfuration pathway and contributes to the majority of HS generation in liver tissues via cysteine metabolism. Dysfunction of the CSE/HS system is linked to both chronic and acute liver damage. This study investigated the regulatory role of CSE deficiency on diethylnitrosamine (DEN)-induced liver damage in mice.
View Article and Find Full Text PDFYakugaku Zasshi
January 2024
Faculty of Pharmacy and Graduate School of Pharmaceutical Sciences, Keio University.
Environmental electrophiles modify thiol groups of proteins in organs, disrupting cellular functions carried out by the modified proteins and increasing the risk of various diseases. The transcription factor NF-E2-related factor 2 (Nrf2) plays a crucial role in detoxifying electrophiles by forming glutathione adducts and subsequently excreting them into extracellular spaces. Supersulfides such as cysteine persulfides (CysSSH) produced by cystathionine γ-lyase (CSE) capture environmental electrophiles through sulfur adduct formation.
View Article and Find Full Text PDFMol Neurobiol
June 2024
Department of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.
The role of hydrogen sulfide (HS) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker C3 protein and assessed the change of BrdU/GFAP-positive cells, GFAP/C3-positive cells, and GFAP/S100a10-positive cells in mice hippocampal tissues to evaluate the change of astrocyte phenotypes following cerebral I/R. The role of HS on the phenotypic change of astrocytes following cerebral I/R in mice was investigated by using HS synthase cystathionine-γ-lyase (CSE) knockout mice (KO).
View Article and Find Full Text PDFEur J Pharmacol
June 2023
Department of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China. Electronic address:
The effect of lipopolysaccharide (LPS)-based neuroinflammation following cerebral ischemia/reperfusion (I/R) on the genotypic transformation of reactive astrocytes and its relationship with endogenous hydrogen sulfide (HS) were investigated in present study. We found that LPS promoted the cerebral I/R-induced A1 astrocytes proliferation in mouse hippocampal tissues and deteriorated the reduction of hydrogen sulfide (HS) content in mouse sera, HS donor NaHS could inhibit A1 astrocytes proliferation. Similarly, knockout of cystathionine γ-lyase (CSE), one of endogenous HS synthases, likewise up-regulated the cerebral I/R-induced A1 astrocytes proliferation, which could also be blocked by NaHS.
View Article and Find Full Text PDFRedox Biol
September 2022
Department of Surgery, University of Texas Medical Branch, Galveston, TX, USA. Electronic address:
Ulcerative colitis (UC) is characterized by widespread relapsing inflammation of the colonic mucosa. Colitis-associated cancer (CAC) is one of the most serious complications of a prolonged history of UC. Hydrogen sulfide (HS) has emerged as an important physiological mediator of gastrointestinal homeostasis, limiting mucosal inflammation and promoting tissue healing in response to injury.
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