Homocysteine and thiol metabolites in vitamin B12 deficiency

摘要: Homocysteine metabolism is increasingly implicated in a diverse group of clinical disorders, including atheromatous vascular disease. We studied the disposition homocysteine via trans-sulphuration pathway, plasma glutathione peroxidase (GPx) activity and levels sulphated hormone dehydro-epiandrosterone sulphate (DHEAS) six vitamin B 12 -deficient human subjects before after 2 weeks repletion, both fasting state following an oral methionine load (0.1 g/kg body weight). Fasting total concentrations fell ( P = 0.03) cysteine rose significantly 0.048) treatment for with injections. The magnitude mean fall concentration (38.8  µ mol/l) was similar to rise (36.0  therapy. Circulating were increased at 4 h when compared levels, repletion 0.003 both). Total cysteinyl-glycine lower post-methionine than therapy 0.007). GPx 0.05). change between loading different pre- post-vitamin present study provides indirect support hypothesis that defects remethylation produce hyperhomocysteinaemia deficiency subjects. Elevated directly or indirectly may up-regulate GPx. Sulphation status, as measured by DHEAS, unchanged.