The toxicity risk of
hyperhomocysteinemia is prevented through
thiol drug administration which reduces plasma total
homocysteine (tHcy) concentrations by activating
thiol exchange reactions. Assuming that
cysteine (Cys) is a
homocysteinemia regulator, the hypothesis was verified in healthy and pathological individuals after the
methionine loading test (MLT). The plasma variations of redox species of Cys, Hcy,
cysteinylglycine,
glutathione and
albumin (reduced, HS-ALB, and at mixed
disulfide, XSS-ALB) were compared in patients with cerebral small vessels disease (CSVD) (n = 11),
multiple sclerosis (MS) (n = 12) and healthy controls (n = 11) at 2-4-6 h after MLT. In MLT-treated subjects, the activation of
thiol exchange reactions provoked significant changes over time in redox species concentrations of Cys, Hcy, and
albumin. Significant differences between controls and pathological groups were also observed. In non-
methionine-treated subjects, total Cys concentrations, tHcy and
thiol-
protein mixed
disulfides (CSS-ALB, HSS-ALB) of CSVD patients were higher than controls. After MLT, all groups displayed significant
cystine (CSSC) increases and CSS-ALB decreases, that in pathological groups were significantly higher than controls. These data would confirm the Cys regulatory role on the
homocysteinemia; they also explain that the Cys-Hcy mixed
disulfide excretion is an important point of
hyperhomocysteinemia control. Moreover, in all groups after MLT, significant increases in
albumin concentrations, named total
albumin (tALB) and measured as sum of HS-ALB (spectrophometric), and XSS-ALB (assayed at HPLC) were observed. tALB increases, more pronounced in healthy than in the pathological subjects, could indicate alterations of
albumin equilibria between plasma and other extracellular spaces, whose toxicological consequences deserve further studies.