Plasma homocysteine as an indicator of folate and vitamin B[12] status in children with acute lymphoblastic leukemia

Folate and vitamin B[12] are important in ensuring proper DNA replication and normal cell division. Their depletion might enhance carcinogenesis. The sulphur containing amino acid homocysteine gained considerable interest as a useful marker of impaired function of folate and vitamin B[12]. The present work aimed to evaluate plasma homocysteine level as a more sensitive indicator of folate and vitamin B[12] status in children with acute lymphoblastic leukemia. This study included fifteen children with newly diagnosed acute lymphoblastic leukemia attending pediatric department of Shatby Hospital, Alexandria University. The control group included fifteen normal healthy volunteers matched for age and sex. In patients, blood samples were collected at the time of diagnosis before any treatment. RBC's folate, plasma folate and vitamin B[12] were estimated using RIA kit. Plasma homocysteine was determined using EIA kit. RBC's folate, plasma folate and vitamin B[12] were significantly lower while plasma homocysteine was significantly elevated in the patient group when compared to the control group. Plasma homocysteine correlated negatively with RBC's folate in both studied groups. This study showed a strong association between folate deficiency, hyperhomocysteinemia and ALL in children. Prospective studies are necessary to further define whether alterations in plasma tHcy and RBC's folate levels can be considered as risk markers or are a consequence of progression of acute lymphoblastic leukemia

Studies of the effect of some schistosomicidal drugs on the vitamin B6 dependent kynurenine hydrolase and kynurenine aminotransferase enzymes in mice

The effect of S. mansoni infected mice with some schistosomicidal drugs: Antimonial e.g., Astiban and non antimonial e.g., Oltipraz and praziquantel on the subsequent metabolism of kynurenine by liver homogentes of mice was studied to explore the effect of both infection and treatment on the B[6] dependent kynurenine hydrolase and kynurenine aminotransferase in the liver homogenates. It could be concluded that infection with S. mansoni created a deficiency in pyridoxal phosphate of the infected mice liver, the B[6] deficiency may induce modified levels of some carcinogenic tryptophan metabolites. This may raise the possibility that these metabolites may be implicated in the high incidence of bladder tumours observed in bilharzial patients [Boyland 1963 and Bryan 1970]. On the other hand, the antibilharzial drugs whether it is antimonial or not cannot completely counteract the disorder in tryptophan metabolism [through the kynurenine pathway] encountered in S. mansoni infected mice