Disease relevance of Dimelor

• We report a case of cholestatic hepatitis accompanied by peripheral and hepatic eosinophilia in a patient taking acetohexamide for a period of 1.5 yr [1].
• We conclude that Cd exposure decreases androgen-dependent metabolism of acetohexamide in liver microsomes of male rats through its testicular toxicity [2].
• In one instance a systemic hypoglycemic reaction resulting in head trauma and confusion ended in an emegency hospital admission following the substitution of acetohexamide for acetazolamide [3].
• Acetohexamide reductase activity in kidney microsomes of male rats was markedly decreased by treatment with Cd at a dose of 1.23 mg/kg body weight [4].
• Severe hypoglycemia in a 67-year-old black male as a result of the ingestion of acetohexamide is described [5].

High impact information on Dimelor

• Based on all results, we conclude that 20beta-hydroxysteroid dehydrogenase catalyzes the ketone-reduction of acetohexamide in liver microsomes of adult male rats [6].
• A variety of patterns of postnatal development were observed for acetohexamide reductase activities in microsomes and cytosols from the liver and kidney of male and female rats [7].
• Carbonyl reductase activity for acetohexamide in human erythrocytes [8].
• Solubilities were predicted within 13% for tolbutamide, 31% for acetohexamide, and 43% for sulfisomidine, and with considerably better accuracy in most solvent mixtures [9].
• This study was designed to elucidate strain- and sex-related differences of carbonyl reductase activity in rat kidney by using the oral antidiabetic drug acetohexamide as substrate [10].

Chemical compound and disease context of Dimelor

• Cadmium exposure decreases androgen-dependent metabolism of acetohexamide in liver microsomes of male rats through its testicular toxicity [2].

Biological context of Dimelor

• Species and sex differences of acetohexamide reductase activity were investigated using the cytosolic fraction of heart homogenate [11].
• Comparative pharmacokinetics of acetohexamide and its metabolite, hydroxyhexamide in laboratory animals [12].
• Studies on drug nonequivalence. VII. Bioavailability of acetohexamide polymorphs [13].
• A simple Mendelian genetic analysis for the frequency distribution of acetohexamide reductase activity in liver microsomes of male rats led us to conclude that the phenotype is genetically regulated by an autosomal co-dominant fashion [14].
• The inheritance patterns of acetohexamide reductase activities in liver microsomes and cytosol of rats were determined by using the inbred Wistar-Imamichi and Fischer-344 strains as a model of low and high metabolizers, respectively [14].

Anatomical context of Dimelor

• Furthermore, a significant correlation was observed between the activities of 20beta-hydroxysteroid dehydrogenase and acetohexamide reductase in liver microsomes of individual male rats at various ages [6].
• Furthermore, acetohexamide reductase activity in erythrocyte was approximately 30% activity of that of human liver (0.17 +/- 0.05 nmol/min/mg cytosolic protein) [8].

Associations of Dimelor with other chemical compounds

• When progesterone was used as a substrate, 20beta-hydroxysteroid dehydrogenase present in liver microsomes of adult rats, such as acetohexamide reductase, exhibited a male-specific and androgen-dependent activity [6].
• We examined the alteration of acetohexamide reductase activities in kidney microsomes and cytosol of cadmium (Cd)-treated rats [4].
• However, oral administration of R-HH to rabbits, in spite of their inability to oxidize R-HH to acetohexamide, caused a significant decrease and increase, respectively, of plasma glucose and insulin levels [15].
• Ketone-containing drugs (daunorubicin, befunolol and levobunolol) other than acetohexamide were little reduced in the cytosol of rabbit heart [11].
• Metabolic reduction of acetohexamide in rat kidney: sex difference and effect of streptozotocin-induced diabetes [16].

Gene context of Dimelor

• Testosterone secreted from the testes during puberty appeared to have a significant effect similar to neonatal imprinting in the induction of acetohexamide reductase activity in liver microsomes of female rats [17].

Analytical, diagnostic and therapeutic context of Dimelor

• Since the reductive metabolism of acetohexamide is known to be reversible in rats, oral administration of R-HH may exhibit the hypoglycemic effect through the generation of acetohexamide [15].
• Acetohexamide hypoglycemia: treatment by peritoneal dialysis [18].
• Factors affecting acetohexamide reductase activities in microsomes and cytosol from the kidney of male rats: age and castration [19].
• The in vivo and in vitro bindings of (-)-hydroxyhexamide, a major metabolite of acetohexamide, to rabbit serum were examined by using an ultrafiltration method [20].
• A major metabolite of acetohexamide was isolated in 41.5% yield from the enzyme reaction mixture, and identified as (-)-hydroxyhexamide by techniques including the melting point, thin-layer chromatography, infrared spectrometry and optical rotation [21].

References