Cobalt-deficiency-induced hyperhomocysteinaemia and oxidative status of cattle

In ruminants, Co is required for the synthesis of vitamin B-12, which in tu rn is needed for the resynthesis of methionine by methylation of homocystei ne and thus, cobalamin deficiency may induce hyperhomocysteinaemia which is brought into context with perturbations of the antioxidative-prooxidative balance. The present study was conducted to explore whether Co deficiency i n cattle is also associated with homocysteine-induced disturbances of oxida tive status. Co deficiency was induced in cattle by feeding two groups of a nimals on either a basal maize-silage-based diet that was moderately low in Co (83 mu g Co/kg DM), or the same diet supplemented with Co to a total of 200 mu g Co/kg DM, for 43 weeks. Co deficiency was apparent from a reduced vitamin B-12 status in serum and liver and an accumulation of homocysteine in plasma which was in excess of 4.8 times higher in Go-deprived cattle th an in controls. The much increased level of circulating homocysteine did no t indicate severe disturbances in antioxidant-prooxidant balance as measure d by individual markers of lipid peroxidation, protein oxidation, and the a ntioxidative defence system. There were no quantitative difference in plasm a thiol groups, nor were there significant changes in concentrations of alp ha-tocopherol, microsomal thiobarbituric acid-reactive substances and carbo nyl groups in liver. However, there was a trend toward increased plasma car bonyl levels indicating a slight degradation of plasma proteins in the hype rhomocysteinaemic cattle. Analysis of the hepatic catalase (EC 1.11.1.6) ac tivity revealed an 11% reduction in Co-deficient cattle relative to the con trols. These results indicate that long-term moderate Co deficiency may ind uce a severe accumulation of plasma homocysteine in cattle, but considerabl e abnormalities in oxidative status failed to appear.