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Effect of folic acid and vitamin B12 administration on phenytoin induced toxicity in rats

机译:叶酸和维生素B12给药对苯妥英钠致大鼠毒性的影响

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摘要

Folic acid and vitamin B12 are very important vitamins needed for normal cellular metabolic activities. The effects of folic acid and vitamin B12 on liver integrity of growing Wistar albino rats following therapeutic dose of phenytoin administration were investigated. The activities of serum AST, ALT, ALP were investigated. Serum total protein level and lipid profile were also measured as indices of biochemical changes. The ingestion of phenytoin alone in rats significantly reduced serum protein while AST, ALT activities incresed as compared to the control (P<0.05). Supplementation of phenytoin with oral administration of 70microgram/kg body wt of folic acid resulted in a significant reversal in serum total protein and suppression in serum AST and ALT activities. Vitamin B12 supplementation did not afford any significant protection against the effect of phenytoin ingestion but rather phenytoin toxicity was exacerbated in this study. However, the combined effects of vitamin B12 and folic acid ameliorated the effects of phenytoin on serum enzymes of experimental rats. The effect of combination of phenytoin with folic acid or folic acid and vitamin B12 is an interesting finding. Supplementation of phenytoin with folic acid or combination of these vitamins may be recommended for the purpose of ameliorating the adverse biochemical changes which are associated with phenytoin therapy. Further work is ongoing to help elucidate the effects of phenytoin and these vitamins on oxidative stress inducing mechanism.
机译:叶酸和维生素B12是正常细胞代谢活动所需的非常重要的维生素。研究叶酸和维生素B12对治疗剂量的苯妥英钠给药后生长的Wistar白化病大鼠肝脏完整性的影响。研究了血清AST,ALT,ALP的活性。血清总蛋白水平和脂质谱也被测量为生化变化的指标。与对照组相比,单独摄入苯妥英钠可显着降低血清蛋白,而AST,ALT活性则增加(P <0.05)。口服每公斤体重70微克苯酚补充苯妥英钠可导致血清总蛋白显着逆转,并抑制血清AST和ALT活性。补充维生素B12不能有效抵抗苯妥英钠的摄入,但在这项研究中苯妥英钠的毒性加剧了。然而,维生素B12和叶酸的联合作用改善了苯妥英钠对实验大鼠血清酶的影响。苯妥英钠与叶酸或叶酸和维生素B12组合的作用是一个有趣的发现。为了减轻与苯妥英治疗有关的不利的生化变化,可能建议补充叶酸或这些维生素的组合的苯妥英钠。正在进行进一步的工作以帮助阐明苯妥英和这些维生素对氧化应激诱导机制的作用。

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