Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:4.2.1.22 (
cystathionine beta-synthase
)
965
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The addition of L-cysteine to hepatic cytosols causes inactivation of
tyrosine aminotransferase
. We have studied the mechanism of inactivation and the effect of streptozotocin-induced diabetes in the rat on the inactivation of
tyrosine aminotransferase
in the presence of fractions prepared from livers and kidneys. Diabetes increased the rate at which
tyrosine aminotransferase
was inactivated after addition of cysteine to hepatic cytosols. The inactivation was due to the production of thiocysteine (which contains sulfane sulfur) from cystine as a result of desulfuration catalyzed by gamma-cystathionase. Diabetes increased the content of
cystathionine beta-synthase
and gamma-cystathionase in liver. As a result, cytosols from diabetic animals converted homocysteine, cystathionine, cysteine and cystine to sulfane at an elevated rate, with resulting inactivation of
tyrosine aminotransferase
. In contrast, inactivation in kidney fractions was not affected by diabetes. Incubation with an inhibitor of gamma-cystathionase (propargylglycine) prevented inactivation of
tyrosine aminotransferase
. These results show that the potential for the formation of sulfane sulfur by the enzymes of the transsulfuration pathway is enhanced by chronic diabetes.
...
PMID:Experimental diabetes increases the formation of sulfane by transsulfuration and inactivation of tyrosine aminotransferase in cytosols from rat liver. 256 58
