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755 Mechanistically, SSAT1 overexpression increases ALOX15 expression and decreases the expression levels of GPX4 and SLC7A11 in primary cortical neurons, suggesting that SSAT1/ALOX15 axis activation may aggravate brain I/R injury by triggering ferroptosis in neurons

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No adverse sequelae developed in the three viable infants

However, very limited information is available about the exact metabolic functions of disease-induced GST isoenzymes and about their endogenous substrates

However, one study on the treatment of children with methylmalonic acidemia and homocystinuria found oral hydroxocobalamine at 1 mg daily to be ineffective in reducing levels of homocysteine