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Phenytoin serum enzymes lipid profile vitamin B12 atherosclerosis hepatotoxicity
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©Nigerian Society for Experimental Biology
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Vitamin b12 supplementation: effects on some biochemical and haematological indices of rats on phenytoin administration
Abstract
Phenytoin is known to have some toxicological implications. Vitamin B12 supplementation during phenytoin administration was investigated to assess the benefits and risks of single vitamin supplementation. This study evaluated the biochemical and haematological effects of vitamin B12 on phenytoin toxicity. Twenty-four experimental animals were divided into 3 groups of 8 rats each. The control (group 1) received distilled water as placebo. Groups 2 and 3 were given 5mg/kg body weight of phenytoin for 4 weeks while group 3 in addition to
phenytoin received intra-peritoneal administration of 15g/kg body of vitamin B12 twice a week. Biochemical parameters such as AST, ALT, ALP, lipid profile and haematological indices were assayed as indices of toxicity. The result of the study showed that phenytoin administration resulted in anaemia which was ameliorated by vitamin
B12 co-administration. Phenytoin also increased significantly the leukocyte count upon which B12 had no effect. Liver enzymes activities were significantly (p<0.05) raised during phenytoin administration and interestingly B12 further increased the level of these enzymes. Administration of phenytoin only gave a significant (p<0.05) increase
in the level of serum Low density lipoprotein cholesterol. Serum cholesterol, TG and HDL-chol were not significantly affected. Although there was no significant change in serum cholesterol, the slight increase was more than 1% which is capable of causing a 3% increase in the risk of coronary heart disease. A significant decrease was
also noted when phenytoin was supplemented with B12. We observed that vitamin B12 co-administration is beneficial in remitting anaemia and the atherosclerotic risk caused by phenytoin but may enhance hepatotoxicity. By this result we would therefore suggest that the use of vitamin B12 alone as supplement during phenytoin administration be discouraged.
phenytoin received intra-peritoneal administration of 15g/kg body of vitamin B12 twice a week. Biochemical parameters such as AST, ALT, ALP, lipid profile and haematological indices were assayed as indices of toxicity. The result of the study showed that phenytoin administration resulted in anaemia which was ameliorated by vitamin
B12 co-administration. Phenytoin also increased significantly the leukocyte count upon which B12 had no effect. Liver enzymes activities were significantly (p<0.05) raised during phenytoin administration and interestingly B12 further increased the level of these enzymes. Administration of phenytoin only gave a significant (p<0.05) increase
in the level of serum Low density lipoprotein cholesterol. Serum cholesterol, TG and HDL-chol were not significantly affected. Although there was no significant change in serum cholesterol, the slight increase was more than 1% which is capable of causing a 3% increase in the risk of coronary heart disease. A significant decrease was
also noted when phenytoin was supplemented with B12. We observed that vitamin B12 co-administration is beneficial in remitting anaemia and the atherosclerotic risk caused by phenytoin but may enhance hepatotoxicity. By this result we would therefore suggest that the use of vitamin B12 alone as supplement during phenytoin administration be discouraged.
