Protective roles of transsulfuration against methionine toxicity

Shotaro Kamata, Isao Ishii

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Citations (Scopus)


Methionine is an essential amino acid in mammals, but is the most toxic among the constituent amino acids of proteins. Excessive methionine intake causes oxidative/nitrosative injuries in the liver, hepatic/splenic hypertrophy, altered erythrocyte morphology, and the resultant splenic hemosiderosis in rats; however, the pathophysiology of methionine-induced liver toxicity remains to be elucidated. Methionine can be metabolized into cysteine by methionine cycle and transsulfuration, and cysteine can be further metabolized into cytoprotective metabolites such as glutathione, taurine, and hydrogen sulfide (H2S). We recently found that a methionine-rich diet induces acute lethal hepatitis in transsulfuration-defective cystathionine γ-lyase-deficient mice. Molecular mechanisms by which methionine excess induces hepatic dysfunction and physiological roles of transsulfuration in its detoxification (metabolism) are herein reviewed.

Original languageEnglish
Title of host publicationMethionine
Subtitle of host publicationBiosynthesis, Chemical Structure and Toxicity
PublisherNova Science Publishers, Inc.
Number of pages11
ISBN (Print)9781626182462
Publication statusPublished - 2013 Apr 1

ASJC Scopus subject areas

  • General Biochemistry,Genetics and Molecular Biology


Dive into the research topics of 'Protective roles of transsulfuration against methionine toxicity'. Together they form a unique fingerprint.

Cite this