Mathuros RuchirawatChuthaporn Akathos2025-02-032025-02-03198820251988Thesis (M.Sc. (Toxicology))--Mahidol University, 1988https://repository.li.mahidol.ac.th/handle/123456789/103266Toxicology (Mahidol University 1988)The DMN-demethylase system in rat kidney microsomes consisted of at least two isozymes designated as DMN-demethylase I and DMN-demethylase II which operated at low concethration (4-50 mM) and high concentration of DMN (above 50 mM) respectively. The optimum substrate concentrations determined were 4 mM for DMN-demethylase I and 200 mM for DMN-demethylase II. The activity of DMN-demethylase I and DMN-demethylase II of kidney microsomes were only 11% and 16% of the liver enzymes, respectively. In the kidney enzyme system, phenobarbital pretreatment had no effect on DMN-demethylase I and DMN-demethylase II activities. While 3-MC pretreatment incresed both DMN-demethlase I (37%) and DMN-demethylase II (30%). Thiamine deficiency enhanced both the kidney DMN-demethylase I and DMN-demethylase II activities. This effect is different from that of the liver system in which thiamine deficiency markedly enhanced the activity of DMN-demethylase II without a significant effect on DMN-demethylase I. Phenobarbital pretreatment in thiamine deficient rats produced no effects on kidney DMN-demethylase activity as also observed in the controls. For 3-MC pretreatment, only DMN-demethylase II was 22% decreased. Thiamine hydrochloride supplementation could reverse the enhanced effect of thiamine deficiency and this effect was not mediated through the level of TPP in the microsomal enzyme system.x, 106 leaves : ill.application/pdfengผลงานนี้เป็นลิขสิทธิ์ของมหาวิทยาลัยมหิดล ขอสงวนไว้สำหรับเพื่อการศึกษาเท่านั้น ต้องอ้างอิงแหล่งที่มา ห้ามดัดแปลงเนื้อหา และห้ามนำไปใช้เพื่อการค้าDimethylnitrosamine -- MetabolismEnzyme InductionEnzyme InhibitorsThiamine deficiencyMaster ThesisMahidol University