1.1.1.1 alcohol dehydrogenase medicine isozyme ADH2 is a target for anti-amoebic agents 1.1.1.1 alcohol dehydrogenase medicine organ simulations indicate that higher therapeutic acetaminophen (0.5 mM) inhibits 16% of allotype ADH1B*1/*1 hepatic ADH activity at 2-20 mM ethanol and that therapeutic salicylate (1.5 mM) inhibits 30-31% of the allotype ADH1B*2/*2 activity, suggesting potential significant inhibitions of ethanol first-pass metabolism in these allelotypes 1.1.1.2 alcohol dehydrogenase (NADP+) medicine - 1.1.1.2 alcohol dehydrogenase (NADP+) medicine brain aldehyde reductase activity is closely associated with pharmalogical actions of drugs affecting the central nervous system, anti-convulsant drugs have inhibitory effects, more work is needed for the mechanism of action of psychoactive drugs and interactions of barbiturates with aldehyde reductase 1.1.1.2 alcohol dehydrogenase (NADP+) medicine inhibitors alrestatin and sorbinil, possible method of preventing neuropathy and cataractogenesis associated with diabetes 1.1.1.2 alcohol dehydrogenase (NADP+) medicine enzyme as a target for anti-tuberculosis and other drugs 1.1.1.2 alcohol dehydrogenase (NADP+) medicine enzyme may be an interesting target for development of new anti-mycobacterial agents 1.1.1.2 alcohol dehydrogenase (NADP+) medicine drugs for testing function of liver and kidney 1.1.1.2 alcohol dehydrogenase (NADP+) medicine daunorubicin, a cancer chemotherapeutic agent can be reduced by aldehyde reductase 1.1.1.2 alcohol dehydrogenase (NADP+) medicine ability of aldehyde reductase from liver to reduce certain cancer chemotherapeutic antibiotics suggested a role for this enzyme in drug metabolism 1.1.1.8 glycerol-3-phosphate dehydrogenase (NAD+) medicine the hyperthyroid status leads to a significant decrease and the hypothyroid status to a significant increase of both enzyme amount and activity in both female and male animals. The euthyroid and hyperthyroid females show a higher activity and the hyperthyroid females also show a higher enzyme amount in comparison with male animals, while the hypothyroid animals show low levels in both sexes. The enzyme-dependent oxygen consumption of freshly isolated liver mitochondria from hyperthyroid animals is higher compared with euthyroid animals, and is activated bycoenzyme Q analogue idebenone, in both euthyroid and hyperthyroid rats. Determination of enzyme amount and activity can serve as an additional criterion for the evaluation of the thyroid hormone status 1.1.1.8 glycerol-3-phosphate dehydrogenase (NAD+) medicine pomolic acid suppresses the increase in GPDH activity in adipocytes when 3T3-L1 cells are treated with pomolic acid during culture in an insulin-containing medium after induction of differentiation. Pomolic acid promotes an increase in GPDH activity in differentiated 3T3-L1 adipocytes when these cells are treated with pomolic acid during culture in the differentiation medium 1.1.1.8 glycerol-3-phosphate dehydrogenase (NAD+) medicine the mRNA expression level of glycerol-3-phosphate dehydrogenase (GPD1) is significantly downregulated in human breast cancer patients. Patients with reduced GPD1 expression exhibit poorer overall metastatic relapse-free survival. The reduced expression of GPD1 is an independent predictor of overall survival in oestrogen receptor-positive and nodal-negative breast cancer patients. GPD1 is a direct target of miR-370, which is significantly upregulated in human breast cancer. Exogenous expression of GPD1 in MCF-7 and MDA-MB-231 breast cancer cells significantly inhibits cell proliferation, migration, and invasion 1.1.1.14 L-iditol 2-dehydrogenase medicine target for inhibitor design 1.1.1.14 L-iditol 2-dehydrogenase medicine target for inhibitor design in hyperglycaemia and diabetes mellitus treatment 1.1.1.21 aldose reductase medicine enzyme protein levels and activity decrease progressively during heart failure upon rapid left ventricular pacing, such as myocardial capacity to detoxify lipid-peroxidation derived aldehydes 1.1.1.21 aldose reductase medicine inhibition of enzyme by tolrestat or sorbinil prevents apotosis and activation of calpase-3, attenuation of TNF-alpha and hyperglykemia-induced activation of protein kinase C, but does not prevent the activation of transkription factor NK-kappaB and protein kinase C by phorbol ester, enzyme is an obligatory mediator of the apoptotic events upstream of protein kinase C 1.1.1.21 aldose reductase medicine inhibition of enzyme by zolrestat attenuates apoptosis in sorbitol-treated cells. Hyperosmolarity-induced cell death requires induction of enzyme as well as a decrease in intracellular glutathione levels 1.1.1.21 aldose reductase medicine inhibition of enzyme inhibits vascular smooth muscle cell growth upon injuries via a decrease in activity of transcription factor NF-kappaB 1.1.1.21 aldose reductase medicine inhibition of enzyme prevents TNF-alpha-induced increase in Bax and Bak and the downregulation of Bcl-2, inhibition abrogates Ap-1 DNA binding activity and prevents the activation of caspase-3, JNK, and p38 MAPK in cells stimulated by TNFalpha 1.1.1.21 aldose reductase medicine myocardial enzyme activity is increased during ischemia, partially due to activation by nitric oxide, enzyme inhibition increases glycolysis and glucose oxidation 1.1.1.21 aldose reductase medicine pharmacological inhibition of enzyme significantly reduces ischemic injury and improves functional recovery in enzyme transgenic mice 1.1.1.21 aldose reductase medicine inhibition of AR may assist in the chemotherapy of malignant tumors by suppressing the rapid growth of cancer cells 1.1.1.21 aldose reductase medicine inhibition of AR may be a significant therapeutic approach in preventing bacterial endotoxin-induced sepsis and tissue damage 1.1.1.21 aldose reductase medicine in streptozotocin-diabetic mice, aldose reductase inhibitor treatment or genetic deficiency of aldose reductase result in significant dephosphorylation of both peroxisome proliferator-activated receptor alpha and ERK1/2 1.1.1.21 aldose reductase medicine inhibition of enzyme in neural stem cells exposed to high glucose concentration results in decrease of oxidative stress, restoration of cell viability and proliferation, and reduction of apoptotic cell death. Inhibition attenuates the down-regulation of glucose transporter 1 expression 1.1.1.21 aldose reductase medicine inhibition/antisense abolition of aldose reductase inhibits the tumor necrosis factor alpha-induced synthesis of prostaglandin E2 and the activity of cyclooxygenase. Inhibition of aldose reductase prevents tumor necrosis factor alpha-induced activation of protein kinase C and NF-kappaB which results in the abrogation of Cox-2 mRNA and protein expression 1.1.1.21 aldose reductase medicine treatment with the nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester prevented ischemia-induced aldose reductase activation and myocardial sorbitol accumulation in rat hearts subjected to global ischemia ex vivo or coronary ligation in situ, whereas inhibition of inducible nitric oxide synthase and neuronal nitric oxide synthase have no effect. Activation of aldose reductase in the ischemic heart is abolished by pretreatment with peroxynitrite scavengers hesperetin or 5,10,15,20-tetrakis-[4-sulfonatophenyl]-porphyrinato-iron [III] 1.1.1.21 aldose reductase medicine ALR2 is a critical target to prevent and control diabetic complications through the inhibition of its activity 1.1.1.21 aldose reductase medicine inhibition of aldose reductase may represent a useful strategy for treating vascular inflammation associated with diabetes 1.1.1.21 aldose reductase medicine levels of ALR2 activity as well as sorbitol in erythrocytes may have value as a quantitative trait to establish a risk profile for development of diabetic retinopathy, type 2 diabetic patients with diabetic retinopathy show significantly higher specific activity of ALR2 as compared to type 2 diabetic patients without diabetic retinopathy 1.1.1.21 aldose reductase medicine aldose reductase ALR2 is a target enzyme for the treatment of diabetic complications 1.1.1.21 aldose reductase medicine the enzyme may be a potential drug target or vaccine candidate for schistosomes 1.1.1.21 aldose reductase medicine fidarestat decreases doxorubicin-induced upregulation of CD11b in THP-1 monocytes. Fidarestat attenuates doxorubicin-induced upregulation of IL-6, IL-1bta, and Nos2 in murine bone-marrow derived macrophages. Fidarestat also attenuates doxorubicin-induced activation and infiltration of multiple subsets of inflammatory immune cells identified by expression of markers CD11b+, CD11b+F4/80+, Ly6C+CCR2high, and Ly6C+CD11b+ in the mouse spleen and liver. Upregulation of markers of mitochondrial biogenesis PGC-1alpha, COX IV, TFAM, and phosphorylation of AMPKalpha1 (Ser485) is observed in THP-1 cells and livers of mice treated with doxorubicin in combination with fidarestat 1.1.1.21 aldose reductase medicine mice devoid of AKR1B3 and exposed to acute occlusion of the left anterior descending coronary artery display reduced infarct size and improved functional recovery at 48 hours compared to wild-type mice. The cardioprotection observed in AKR1B3 null mice is linked to acute activation of the beta-catenin pathway and consequent activation of mesenchymal markers and genes linked to fibrotic remodeling. The increased activity of the beta-catenin pathway at 48 hours of recovery is not observed at 28 days post-infarction. In ex vivo studies, inhibition of beta-catenin blocks the cardioprotection observed in AKR1B3 null mice hearts 1.1.1.22 UDP-glucose 6-dehydrogenase medicine possibility that gallic acid and quercetin may modulate human breast cancer cell proliferation by inhibiting UGDH 1.1.1.22 UDP-glucose 6-dehydrogenase medicine UGDH content in prostatic acini is a novel candidate biomarker that may complement the development of a multi-biomarker panel for detecting prostate cancer within the tumor adjacent field on a histologically normal biopsy specimen 1.1.1.22 UDP-glucose 6-dehydrogenase medicine manipulation of UGDH activity by hexamer stabilization may offer therapeutic options in cancer and other pathologies 1.1.1.22 UDP-glucose 6-dehydrogenase medicine biallelic mutations in UGDH cause developmental epileptic encephalopathy. In 36 cases from 25 families presenting with epileptic encephalopathy with developmental delay and hypotonia, mutations either impair UGDH stability, oligomerization, or enzymatic activity. In vitro, patient-derived cerebral organoids are smaller with a reduced number of proliferating neuronal progenitors 1.1.1.22 UDP-glucose 6-dehydrogenase medicine epirubicin accumulation increases and apoptosis decreases during UGDH knockdown. Hyaluronan-coated matrix increases and a positive modulation of autophagy is detected. Higher levels of UGDH are correlated with worse prognosis in triple-negative breast cancer patients that receive chemotherapy. High expression of UGDH is found in tumoral tissue from HER2--patients. UGDH knockdown contributes to epirubicin resistance 1.1.1.22 UDP-glucose 6-dehydrogenase medicine expression of UDP-glucose dehydrogenase is up-regulated in highly metastatic ovarian cancer TOV-21G cells, but not in normal adjacent tissue. RNAi-mediated silencing results in a significant decrease in metastatic ability in transwell migration, transwell invasion and wound healing assays. The knockdown of UGDH causes cell cycle arrest in the G0/G1 phase and induces a massive decrease of tumour formation rate in vivo. UGDH-depletion leads to the down-regulation of epithelial-mesenchymal transition-related markers as well as MMP2, and inactivation of the ERK/MAPK pathway 1.1.1.22 UDP-glucose 6-dehydrogenase medicine high UGDH expression is associated with decreased patient survival in poor-prognosis breast cancer subsets 1.1.1.22 UDP-glucose 6-dehydrogenase medicine knocking out UGDH in highly metastatic 6DT-1 breast cancer cells impairs migration ability without affecting in vitro proliferation. UGDH-KO results in significantly decreased metastatic capacity in vivo when the cells are orthotopically injected in syngeneic mice 1.1.1.22 UDP-glucose 6-dehydrogenase medicine shRNA-mediated knockdown of UGDH inhibits breast cancer invasion, colony formation, and tumor growth 1.1.1.26 glyoxylate reductase medicine identification of point mutations and minor deletions resulting in primary hyperoxaluria type 2 1.1.1.27 L-lactate dehydrogenase medicine potential drug target for new antimalarials 1.1.1.27 L-lactate dehydrogenase medicine structural characterization of the enzyme and active-site differences from the human lactate dehydrogenase may be useful for structural-based design of new treatments for toxoplasmic infections 1.1.1.27 L-lactate dehydrogenase medicine suitable drug target for design of novel babesial chemotherapeutics 1.1.1.27 L-lactate dehydrogenase medicine serum LDH zymograms of patients can be used as prognostic marker, since they tend to reach the normal level during recovery signifying the effect of chemotherapy in hospitalized patients. Elevation along with the rise in total LDH activity may be used in the diagnosis and monitoring of tubercular pyothorax 1.1.1.27 L-lactate dehydrogenase medicine the enzyme is a target for treatment of cancer 1.1.1.27 L-lactate dehydrogenase medicine LDH-5 is considered a highly promising target in cancer therapy, LDH-5 significance in the treatment and prognosis of neoplastic diseases 1.1.1.27 L-lactate dehydrogenase medicine LDHB is a therapeutic target in cancer 1.1.1.27 L-lactate dehydrogenase medicine alpha-HBDH is an independent risk factor for systemic lupus erythematosus-related liver injury. alpha-HBDH level is significantly higher in the systemic lupus erythematosus-related liver injury patients than in the non-systemic lupus erythematosus-related liver injury patients. alpha-HBDH is positively correlated with levels of aspartate aminotransferase and lactate dehydrogenase, the aspartate aminotransferase/alanine aminotransferase ratio, and the systemic lupus erythematosus disease activity index 2000, and it is negatively correlated with albumin and C3. The optimal cutoff value of alpha-HBDH for distinguishing systemic lupus erythematosus patients with and without liver injury is 258.50 U/l, which provides a 60.94% sensitivity and a 94.67% specificity 1.1.1.27 L-lactate dehydrogenase medicine alpha-hydroxybutyrate dehydrogenase as an independent prognostic factor for mortality in hospitalized patients with COVID-19. Among 1751 patients with confirmed COVID-19, 15 patients (0.87%) died. The mortality during hospitalization was 0.26% for patients with normal alpha-HBDH levels and 5.73% for those with elevated alpha-HBDH levels 1.1.1.27 L-lactate dehydrogenase medicine HBDH is associated with atherothrombotic events in 83 stable patients undergoing infrainguinal angioplasty and stenting. HBDH levels at baseline are significantly higher in patients who subsequently developed the primary endpoint. HBDH can distinguish between patients without and with future atherothrombotic events. A HBDH concentration at/above 115 U/l is the best threshold to predict the composite endpoint, providing a sensitivity of 83.3% and a specificity of 71.4%, and is therefore defined as high HBDH. Ischemic events occur significantly more often in patients with high HBDH than in patients with lower HBDH levels 1.1.1.29 glycerate dehydrogenase medicine glyoxylate reductase/hydroxypyruvate reductase is a prognostic marker for hepatocellular carcinoma patients after curative resection 1.1.1.34 hydroxymethylglutaryl-CoA reductase (NADPH) medicine the enzyme is a target for intervention in the treatment of hypercholesterolaemia, clinical utility of inhibitors to decrease the levels of atherogenic lipiproteins in patients 1.1.1.34 hydroxymethylglutaryl-CoA reductase (NADPH) medicine dual therapy with the HMG-CoA reductase inhibitor pravastatin and the angiotensin receptor antagonist olmesartan, which produce an additive reduction in cardiomyocyte hypertrophy and cardiac fibrosis after myocardial infarction through different mechanisms, decreases the propensity of the heart to arrhythmogenesis 1.1.1.34 hydroxymethylglutaryl-CoA reductase (NADPH) medicine genistein, eicosapentaenoic acid and docosahexaenoic acid down-regulate reductase activity, primarily through posttranscriptional effects. Diets rich in soy isoflavones and fish oils, therefore, may exert anti-cancer effects through the inhibition of mevalonate synthesis in the breast. Genistein and docosahexaenoic acid, in particular, may augment the efficacy of statins, increasing the potential for use of these drugs in adjuvant therapy for breast cancer 1.1.1.34 hydroxymethylglutaryl-CoA reductase (NADPH) medicine the cholesterol absorption inhibitor ezetimibe profoundly lowers serum cholesterol levels in animals expressing very low rates of hepatic cholesterol synthesis and produces large compensatory increases in hepatic HMG-CoA reductase expression without signifucantly affecting expression of hepatic low density lipoprotein receptors. This indicates that ezitimibe should be most effective in lowering serum cholesterol levels in peaple with low rates of cholesterol synthesis/High rates of cholesterol absorption 1.1.1.34 hydroxymethylglutaryl-CoA reductase (NADPH) medicine treatment with the inhibitor atorvastatin exerts early nephroprotective effects in a rat model of chronic inhibition of nitric axide synthesis 1.1.1.35 3-hydroxyacyl-CoA dehydrogenase medicine HADH protects against excess amino acid-induced insulin secretion 1.1.1.35 3-hydroxyacyl-CoA dehydrogenase medicine lack of Hadh2 activity may impart early developmental problems, leading to embryo lethality. In addition to the 3-hydroxyacyl-CoA dehydrogenase activity, the HSD10 (formerly Hadh2) activity is also relevant to the metabolism and meiotic maturation of oocytes 1.1.1.35 3-hydroxyacyl-CoA dehydrogenase medicine the leptospiral enzyme is an early urinary biomarker of leptospirosis 1.1.1.37 malate dehydrogenase medicine therapy development for sexually transmitted disease of humans 1.1.1.39 malate dehydrogenase (decarboxylating) medicine ME2 as a potentially novel metabolic target for leukemia therapy 1.1.1.40 malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+) medicine enzyme ME2 is a potential target for cancer therapy 1.1.1.40 malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+) medicine isoform ME2 is a potential anticancer target 1.1.1.B40 11beta-hydroxysteroid dehydrogenase (NAD+) medicine exposure of fetus to high levels of synthetic glucocorticoid may have long-lasting effects on the hippocampal expression of hypothalamic-pituitary-adrenal-related genes into adulthood 1.1.1.B40 11beta-hydroxysteroid dehydrogenase (NAD+) medicine squirrel monkeys protect the mineralocorticoid receptor from activation by high cortisol levels in the kidney via upregulation of 11beta-HSD2 activity through increased production of the enzyme 1.1.1.B40 11beta-hydroxysteroid dehydrogenase (NAD+) medicine treatment of rats with dehydroepiandrosterone induces a shift from isoform 11beta-HSD1 to 11beta-HSD2 expression, increasing conversion from active to inactive glucocorticoids 1.1.1.B40 11beta-hydroxysteroid dehydrogenase (NAD+) medicine high-fat fed animals overexpress 11beta-hydroxysteroid dehydrogenase type 2 in subcutaneous but not in retroperitoneal fat. Enzyme mRNA levels strongly correlate in both tissues with different parameters related to obesity, such as body weight, adiposity, and insulin resistance 1.1.1.B40 11beta-hydroxysteroid dehydrogenase (NAD+) medicine 11beta-HSD1 is a drug target for treatment of insulin resistance, diabetes and cardiovascular disease 1.1.1.B40 11beta-hydroxysteroid dehydrogenase (NAD+) medicine age-related reduced 11beta-HSD2 activity contributes to the rising prevalence of arterial hypertension in elderly 1.1.1.B40 11beta-hydroxysteroid dehydrogenase (NAD+) medicine at baseline, mRNA levels are similar in skeletal muscle of diabetic and control sugjects for 11beta-HSD1, 11beta-HSD2, and hexose-6-phosphate dehydrogenase. 11beta-HSD1 activity is reduced in diabetic subjects, while 11beta-HSD2 activity is increased. After application of dexamethasone, 11beta-HSD1 mRNA increases in both groups, whereas 11beta-HSD2 mRNA decreases. 11beta-HSD1 activity increases in diabetic subjects, but not in controls, whereas 11beta-HSD2 activity does not change in either group; mRNA levels are similar in diabetic and control subjects for 11beta-hydroxysteroid dehydrogenase 1 and 11beta-hydroxysteroid dehydrogenase 2. 11beta-Hydroxysteroid dehydrogenase 2-activity is higher in diabetic patients. After treatment with dexamethasone, 11beta-hydroxysteroid dehydrogenase 1-mRNA increases in both groups, whereas 11beta-hydroxysteroid dehydrogenase 2-mRNA decreases. 11beta-Hydroxysteroid dehydrogenase 1-activity increases in diabetic patients, but not in control, whereas 11beta-hydroxysteroid dehydrogenase 2-activity does not change in either group 1.1.1.42 isocitrate dehydrogenase (NADP+) medicine sensitizing effect of NADP+-dependent isocitrate dehydrogenase siRNA on the apoptotic cell death of HeLa cells offers the possibility of developing a modifier of cancer therapy 1.1.1.42 isocitrate dehydrogenase (NADP+) medicine the sensitizing effect of NADP+-dependent isocitrate dehydrogenase siRNA on the apoptotic cell death of HeLa cells offers the possibility of developing a modifier of cancer chemotherapy 1.1.1.42 isocitrate dehydrogenase (NADP+) medicine transfection of HeLa cells with an NADP+-dependent isocitrate dehydrogenase small interfering RNA decreased the activity of IDPm, enhancing the susceptibility of radiation-induced apoptosis. The effect of NADP+-dependent isocitrate dehydrogenaseIDPm small interfering RNA on HeLa cells offers the possibility of developing a modifier of radiation therapy 1.1.1.42 isocitrate dehydrogenase (NADP+) medicine the sensitizing effect of IDPm siRNA and autophagy inhibitor on the ionizing radiation induced apoptotic cell death of glioma cells offers a novel redox-active therapeutic strategy for the treatment of cancer 1.1.1.42 isocitrate dehydrogenase (NADP+) medicine the enzyme is a vaccine candidate against the fish pathogen Edwardsiella tarda infection. The serum of enzyme-vaccinated flounder exhibit the highest bactericidal activity compared with other groups. The recombinant enzyme can enhance the expressions of interferon-gamma, natural killer enhancing factor, interleukin-6, major histocompatibility complex Ialpha, CD4-1 and CD8alpha 1.1.1.44 phosphogluconate dehydrogenase (NADP+-dependent, decarboxylating) medicine - 1.1.1.44 phosphogluconate dehydrogenase (NADP+-dependent, decarboxylating) medicine with a deficiency of 6-phosphogluconate dehydrogenase some reticulocytosis occurs 1.1.1.44 phosphogluconate dehydrogenase (NADP+-dependent, decarboxylating) medicine 6PGDH might be a target for chemotherapy against parasitic infections as trypanosomiasis 1.1.1.44 phosphogluconate dehydrogenase (NADP+-dependent, decarboxylating) medicine 6-phosphogluconate dehydrogenase is a potential target for new drugs against African trypanosomiasis 1.1.1.45 L-gulonate 3-dehydrogenase medicine role in an alternative pathway of the production of xylitol in the lens that causes cataracts in mammalian organisms 1.1.1.49 glucose-6-phosphate dehydrogenase (NADP+) medicine G6PD deficiency due to its polymorphism causes neonatal jaundice, acute hemolysis in malaria, favism, severe chronic non-spherocytic hemolytic anemia, and lipid dysregulation. G6PD deficiency may be responsible for the high incidence of coronary artery disease among African-Americans and reduces mortality due to ischemic heart disease and cerebrovascular disease in Sardinian males. In Mediterranean and Sardinian G6PD-deficient individuals, G6PD deficiency may confer a partial protection against atherosclerosis, leading to a reduced risk of cardiovascular diseases in G6PD-deficient individuals. G6PD appears to be an attractive therapeutic target for diabetes-induced cardiomyopathy, ischemic cardiomyopathy, pulmonary hypertension, angiotensin II-induced hypertension, vascular smooth muscle hypertrophy and coronary disease in humans 1.1.1.49 glucose-6-phosphate dehydrogenase (NADP+) medicine G6PD deficiency is the commonest clinically significant enzymopathy in humans. More than 400 million people worldwide are affected by this condition which may determine favism, drug-induced acute hemolytic anemia, severe chronic nonspherocytic haemolytic anemia, neonatal jaundice and hemolytic anemia associated with viral or microbiological infections. The highest prevalence of G6PD deficiency mainly regards tropical Africa, the Middle East, tropical and subtropical Asia, Papua New Guinea, and various Mediterranean regions, for example Sardinia island. G6PD deficiency may represent a selective advantage due to the increased resistance to severe Plasmodium falciparum infection of the affected individuals. G6PD/pyruvate kinase ratio is more reliable than the G6PD activity alone, for the identification of G6PD heterozygotes, especially in patients with microcytic anemia. G6PD/6PDG ratio is an absolute measure of G6PD deficiency of female carriers 1.1.1.49 glucose-6-phosphate dehydrogenase (NADP+) medicine in Vietnam the blackwater fever syndrome is associated with malaria infection, quinine ingestion and G6PD deficiency. G6PD deficiency is a major risk factor for haemoglobinuria in ethnic Vietnamese Kinh and within the G6PD deficient population G6PD Viangchan is significantly associated with haemoglobinuria 1.1.1.49 glucose-6-phosphate dehydrogenase (NADP+) medicine refolding protocol can be applied to produce high recovery yield of folded protein with unaltered properties, paving the way for future studies on clinical G6PD mutants with folding defects and providing a useful model system to study the folding process of oligomeric proteins 1.1.1.49 glucose-6-phosphate dehydrogenase (NADP+) medicine fluoride-containing bioactive glasses as used in tissue engineering as well as bone repair, inhibit the pentose phosphate oxidative pathway and the glucose 6-phosphate dehydrogenase activity. The effects are ascribable to the fluoride content/release of glass powders, they are mimicked by NaF solutions and are prevented by radical scavengers dimethyl sulfoxide and tempol, by superoxide dismutase, and by glutathione, but not by apocynin 1.1.1.50 3alpha-hydroxysteroid 3-dehydrogenase (Si-specific) medicine enzyme as part of commercial enzyme test kit for bile acid content in serum as an index for hepatic diseases 1.1.1.50 3alpha-hydroxysteroid 3-dehydrogenase (Si-specific) medicine enzyme is a potential drug target 1.1.1.51 3(or 17)beta-hydroxysteroid dehydrogenase medicine inhibitor Strogen forte extract can be used for treatment of benign prostatic hyperplasia 1.1.1.62 17beta-estradiol 17-dehydrogenase medicine binding of equilin at the active site of the enzyme is the basis for inhibition of reduction of estrone to estradiol. One possible outcome of estrogen replacement therapy in vivo can be the reduction of estradiol levels in breast tissues and hence the reduced risk of estrogen-dependent breast cancer 1.1.1.62 17beta-estradiol 17-dehydrogenase medicine attractive drug target in hormone-sensitive breast cancer 1.1.1.62 17beta-estradiol 17-dehydrogenase medicine target for suppression of estrogen synthesis in breast cancer 1.1.1.62 17beta-estradiol 17-dehydrogenase medicine as estradiol stimulates the growth and development of hormone-dependent breast cancer, inhibition of the final step of its synthesis is an attractive target for the treatment of this disease 1.1.1.62 17beta-estradiol 17-dehydrogenase medicine estrogenic response for estrone is enhanced by the local action of HSD17B1 in vivo. Thus the enzyme is a potential target for pharmacological inhibition of estrogen activation. Targeted inhibition of HSD17B1 is a promising therapeutic approach to modulate estrogen response in the target tissue with less severe side effects as compared with antiestrogens 1.1.1.62 17beta-estradiol 17-dehydrogenase medicine type 1 17beta-hydroxysteroid dehydrogenase is an interesting biological target for designing drugs for the treatment of estrogen-sensitive diseases such as breast cancer 1.1.1.62 17beta-estradiol 17-dehydrogenase medicine 17beta-HSD1 inhibitors such as STX1040 may provide a treatment for hormone-dependent breast cancer