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PubMed2003

Dose-dependent protective effect of selenium in rat model of Parkinson's disease: neurobehavioral and neurochemical evidences.

Normal cellular metabolism produces oxidants that are neutralized within cells by antioxidant enzymes and other antioxidants. An imbalance between oxidant and antioxidant has been postulated to lead the degeneration of dopaminergic neurons in Parkinson's disease. In this study, we examined whether selenium, an antioxidant, can prevent or slowdown neuronal injury in a 6-hydroxydopamine (6-OHDA) model of Parkinsonism. Rats were pre-treated with sodium selenite (0.1, 0.2 and 0.3 mg/kg body weight) for 7 days. On day 8, 2 micro L 6-OHDA (12.5 micro g in 0.2% ascorbic acid in normal saline) was infused in the right striatum. Two weeks after 6-OHDA infusion, rats were tested for neurobehavioral activity, and were killed after 3 weeks of 6-OHDA infusion for the estimation of glutathione peroxidase, glutathione-S-transferase, glutathione reductase, glutathione content, lipid peroxidation, and dopamine and its metabolites. Selenium was found to be successful in upregulating the antioxidant status and lowering the dopamine loss, and functional recovery returned close to the baseline dose-dependently. This study revealed that selenium, which is an essential part of our diet, may be helpful in slowing down the progression of neurodegeneration in parkinsonism.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Hydroperoxides can modulate the redox state of pyridine nucleotides and the calcium balance in rat liver mitochondria.

When rats are fed a selenium-deficient diet, the glutathione peroxidase activity in liver mitochondria decreases within 5 weeks to 0-6% of that of control animals fed on a diet supplemented with 0.5 ppm of selenium as sodium selenite. Analysis of the temperature dependence of energy-linked Ca(2+) uptake by means of Arrhenius plots reveals two breaks (at around 11 degrees C and 24 degrees C) in mitochondria isolated from selenium-supplemented animals, whereas in selenium-deficient rats the break at 11 degrees C is absent. Ca(2+)-loaded mitochondria of selenium-supplemented rats-i.e., with active glutathione peroxidase in the matrix-lose Ca(2+) rapidly, with a concomitant oxidation of endogenous NAD(P)H, when exposed to t-butyl hydroperoxide or H(2)O(2). In contrast, in selenium deficiency, t-butyl hydroperoxide and H(2)O(2) induce neither a release of Ca(2+) nor an oxidation of NAD(P)H. The peroxide-induced oxidation of NAD(P)H is reversible in the presence of succinate when no Ca(2+) has been taken up. When Ca(2+) has previously been accumulated, however, the oxidation of NAD(P)H is irreversible. Enzymatic analysis of mitochondrial pyridine nucleotides reveals that the peroxide-induced oxidation of NAD(P)H in Ca(2+)-loaded mitochondria leads to a loss of NAD(+) and NADP(+). It is proposed that the redox state of mitochondrial pyridine nucleotides can be or is in part controlled by glutathione peroxidase and glutathione reductase and is a factor in the balance of Ca(2+) between mitochondria and medium.

Animals↗
PubMedDate not supplied

Influence of dietary selenium supplementation and exercise on thiol-containing enzymes in mice.

OBJECTIVE: Exercise markedly increases oxygen uptake by active muscles and consequently increases generation of reactive oxygen species. A dietary deficiency in selenium (Se) can increase the sensitivity of the living system to oxidative stress. delta-Aminolevulinate dehydratase (delta-ALA-D), succinate dehydrogenase (SDH), and lactate dehydrogenase (LDH) are sulfhydryl-containing enzymes, and their activities are sensitive to the presence of oxidizing agents. We investigated the effect of Se deficiency and supplementation on delta-ALA-D, SDH, and LDH activities in mice subjected to swim training for 8 wk. METHODS: Three-month-old female mice were randomly assigned and fed a basal diet, a basal diet plus 1 ppm of Se, and a basal diet plus 40 ppm of Se. These groups were further divided into sedentary and swim-trained groups. A mass equivalent of 5% of the animal's body weight was fixed to the tail. Animals were then exercised for 60 min/d, 4 d/wk. RESULTS: Swim-training associated with Se-deficient diet diminished delta-ALA-D activity in the livers and kidneys. SDH activity was diminished in the skeletal and cardiac muscles of this group. CONCLUSIONS: These results indicated that exercise associated with dietary Se deficiency can inhibit the production of thiol-containing enzymes, delta-ALA-D and SDH, from different tissues; however, LDH activity was not changed. The decrease in enzyme activities can be tentatively attributed to oxidation of thiol groups by the reactive oxygen species produced by exercise.

Animals↗
PubMed1976

Oxidation of S-e-carboxymethyl-selenocysteine by L-aminoacid oxidase and by D-aspartate oxidase.

Se-Carboxymethyl-DL-selnocysteine (CMSeC) has been prepared in a pure crystalline form from selenocysteine and monochloracetic acid. It has been shown that CMSeC is a substrate for the L-aminoacid oxidase form snake venom and for the D-aspartate oxidase from beef kidney. Oxygen consumption and ammonia production indicate that only the L or the D form of CMSeC ar acted upon respectively by one or the other of the above enzymes. No noticeable differences were shown in the oxidation rate of CMSeC and S-carboxymethylcysteine, an indication that the substitution of a selenium for a sulfur atom in the molecule does not greatly affect the substrate specificity of the two enzymes. Data have been obtained suggesting that the product of the oxidative deamination of CMSeC Is Se-carboxymethyl-selenopyruvic acid.

Amino Acid Oxidoreductases↗
PubMed2004

[Metabolic aspects of endotoxin as a model of septic shock--approached from oxidative stress].

Despite the remarkable progress in intensive care medicine, sepsis and shock continue to be major clinical problems in intensive care units. Septic shock may be associated with a toxic state initiated by the stimulation of monocytes by bacterial toxins such as endotoxin, which is released into the bloodstream. This study describes the role of oxidative stress in endotoxin-induced metabolic disorders. We demonstrate that endotoxin injection results in lipid peroxide formation and membrane injury in experimental animals, causing decreased levels of free radical scavengers or quenchers. Interestingly, it was also suggested that tumor necrosis factor (TNF)-induced oxidative stress occurs as a result of bacterial or endotoxin translocation under conditions of reduced reticuloendothelial system function in various disease states. In addition, we suggest that intracellular Ca2+, Zn2+, or selenium levels may participate, at least in part, in the oxidative stress during endotoxemia. On the other hand, it is also suggested that the extent of endotoxin-induced nitric oxide (NO) formation may be due, at least in part, to a change in heme metabolic regulation during endotoxemia. However, in our experimental model, NO is not crucial for lipid peroxide formation during endotoxemia. Sho-saiko-to is one of the most frequently prescribed Kampo medicines and has primarily been used to treat chronic hepatitis. We report that Sho-saiko-to decreases the rh TNF-induced lethality in galactosamine-hypersensitized mice and protects mice against oxygen toxicity and Ca2+ overload in the cytoplasm or mitochondria during endotoxemia. We further suggest that Sho-saiko-to shows a suppressive effect on NO generation in macrophages stimulated with endotoxin and that it may be useful in improving endotoxin shock symptoms.

Animals↗
PubMed1987

Oxidative damage to DNA and replicative lifespan in cultured adrenocortical cells.

Oxidative damage to DNA in cultured bovine adrenocortical cells was investigated by exposing cells to a sublethal concentration (10 microM) of cumene hydroperoxide under conditions previously shown to be deficient in the biological antioxidants selenium and alpha-tocopherol (vitamin E). DNA prepared from cells incubated for 4 h with 10 microM cumene hydroperoxide had a greater fraction showing resistance to S1 nuclease after denaturation and reassociation to a log C0t of -3. Cross-linking by cumene hydroperoxide was abolished in cells that had been grown in the presence of 20 nM selenite or 1 microM alpha-tocopherol for 96 h prior to peroxide addition, whereas such cells remained susceptible to cross-linking by nitrogen mustard. Extensive strand breaks in DNA from peroxide-treated cells as assessed by alkaline sucrose gradient centrifugation were greatly reduced in cells grown in selenite or alpha-tocopherol. Despite the evidence of damage to DNA, cumene hydroperoxide was not detectably mutagenic, in contrast to 5 microM methylnitronitrosoguanidine (MNNG), when assessed as the incidence of resistance to 25 microM ouabain. We confirmed that cumene hydroperoxide at greater than 10 microM lowers cloning efficiency and that this is largely prevented by selenite or alpha-tocopherol. Additionally, selenite or alpha-tocopherol produced increased clonogenicity in cells not incubated with peroxide. To examine effects of the biological antioxidants on replicative lifespan, cells were grown continuously in fetal bovine serum (FBS), fibroblast growth factor (FGF), and selenite or alpha-tocopherol. Selenium increased replicative lifespan by 10-20% and alpha-tocopherol by 22-30%. Levels of DNA cross-links and strand breaks did not differ under any circumstances between early (second) passage and late (30th) passage cells. The experiments on replicative potential were all performed in the presence of FGF. When FGF was omitted from the culture medium, replicative lifespan was reduced by 85%. We conclude that types of damage to DNA resulting from peroxide exposure are not present in cells under standard culture conditions at early or late stages of the lifespan. Other work has noted a relationship between clonogenicity and replicative lifespan; thus, the increase in cloning efficiency seen with selenium and alpha-tocopherol may cause the observed slight increase in replicative lifespan. Oxidative damage does not appear to be a major determinant of cellular senescence in adrenocortical cells.

Adrenal Cortex↗
PubMed1979

Effects of vitamin E and selenium deficiency on the fatty acid composition of rat retinal tissues.

The fatty acid composition of retinal tissues was measured in rats maintained for 26--32 weeks on each of the following diets: a purified basal diet deficient in alpha-tocopherol and selenium, an identical control diet supplemented with alpha-tocopherol and selenium, and a commerical laboratory rat chow. Dietary deficiencies of antioxidant nutrients were found to cause a large decrease in total polyunsaturated fatty acids in the retinal pigment epithelium, a small decrease in the retinal rod outer segments, but no change in the whole retina or liver when compared to tissues from animals fed the vitamin E- and selenium-supplemented control diet. The polyunsaturated fatty acid content which we have observed for the retinal pigment epithelium from rats fed commerical lab chow is similar to that which we observed for bovine retinal pigment epithelium. Our results indicate that changes in fatty acid composition are not generalized to all tissues in severely antioxidant-deficient animals, but that changes do occur in some tissues, such as the retinal pigment epithelium, which appears to be particularly sensitive to in vivo lipid peroxidation.

Animals↗
PubMed1985

Effect of selenium deficiency on hydroperoxide-induced glutathione release from the isolated perfused rat heart.

Selenium deficiency has been implicated as a cause of the cardiomyopathy known as Keshan disease in China. Selenium is an essential constituent of glutathione peroxidase, an enzyme that destroys hydroperoxides by using the reducing equivalents of reduced glutathione (GSH). We studied glutathione-dependent hydroperoxide metabolism in isolated perfused rat hearts. Hearts from selenium-deficient rats contained 5% of the glutathione peroxidase activity found in control hearts. Glutathione reductase activity and glutathione content were not affected by selenium deficiency. Infusion of t-butylhydroperoxide into control hearts caused an increase in heart glutathione disulfide (GSSG) concentration proportional to the rate of hydroperoxide infusion up to 200 nmol/(g heart X min). GSSG was released into the perfusate in proportion to the hydroperoxide infusion rate up to 150 nmol/(g heart X min), but GSSG release did not increase further with higher infusion rates. Thus, GSSG release by the heart is saturable. It had a maximum rate of about 14 nmol GSH equivalents/(g heart X min) when stimulated by t-butylhydroperoxide infusion. This indicates that GSSG release by the heart is carrier-mediated and is not due to passive diffusion. Infusion of hydroperoxide into selenium-deficient hearts failed to cause increases in heart GSSG concentration and in GSSG release. This indicates that selenium-deficient heart cannot metabolize hydroperoxides through glutathione-dependent pathways. We suggest that selenium deficiency might predispose the heart to injury from oxidant stress.

Animals↗
PubMed1999

The crystal structure of a reduced [NiFeSe] hydrogenase provides an image of the activated catalytic center.

BACKGROUND: [NiFeSe] hydrogenases are metalloenzymes that catalyze the reaction H2<-->2H+ + 2e-. They are generally heterodimeric, contain three iron-sulfur clusters in their small subunit and a nickel-iron-containing active site in their large subunit that includes a selenocysteine (SeCys) ligand. RESULTS: We report here the X-ray structure at 2.15 A resolution of the periplasmic [NiFeSe] hydrogenase from Desulfomicrobium baculatum in its reduced, active form. A comparison of active sites of the oxidized, as-prepared, Desulfovibrio gigas and the reduced D. baculatum hydrogenases shows that in the reduced enzyme the nickel-iron distance is 0.4 A shorter than in the oxidized enzyme. In addition, the putative oxo ligand, detected in the as-prepared D. gigas enzyme, is absent from the D. baculatum hydrogenase. We also observe higher-than-average temperature factors for both the active site nickel-selenocysteine ligand and the neighboring Glu18 residue, suggesting that both these moieties are involved in proton transfer between the active site and the molecular surface. Other differences between [NiFeSe] and [NiFe] hydrogenases are the presence of a third [4Fe4S] cluster replacing the [3Fe4S] cluster found in the D. gigas enzyme, and a putative iron center that substitutes the magnesium ion that has already been described at the C terminus of the large subunit of two [NiFe] hydrogenases. CONCLUSIONS: The heterolytic cleavage of molecular hydrogen seems to be mediated by the nickel center and the selenocysteine residue. Beside modifying the catalytic properties of the enzyme, the selenium ligand might protect the nickel atom from oxidation. We conclude that the putative oxo ligand is a signature of inactive 'unready' [NiFe] hydrogenases.

Amino Acid Sequence↗
PubMed1987

Variations among cultured cells in glutathione peroxidase activity in response to selenite supplementation.

The aim of this study was to devise conditions for manipulation of the activity of selenium-dependent glutathione peroxidase in cell lines by means of variation in culture medium contents of selenite and fetal calf serum. Nine different cell lines were studied. A low glutathione peroxidase activity was, in most cases, obtained by the use of a medium with a low (2%) serum content. Selenite induced in most of the cell lines an increase in glutathione peroxidase activity, with a plateau ranging from 10 nM to 300-1000 nM. Growth-retarding effects of selenite became apparent at 300-2000 nM, showing a large cell line variation. Supplementation with 50-100 nM selenite for 1 week should generally be suitable for maximal glutathione peroxidase induction. The selenium contents of serum batches were highly variable, pointing to the importance of using only one well-defined, preferably low-selenium, batch. The glutathione peroxidase activities varied considerably between cell lines and the selenite-induced increases ranged from negligible to more than 10-fold. The availability of cell lines with such variable responses should be valuable for experiments aimed at evaluating the importance of glutathione peroxidase and selenium compounds independently of glutathione peroxidase for the protection against oxidative insult.

Cell Division↗
PubMed1995

Effect of selenium in recovery of immunity damaged by H2O2 and 60Co radiation.

Con A stimulated lymphocytes proliferation was measured as [3H]thymidine incorporation and IgG was quantified by single radial immunodiffusion to study recovering or protecting effect of selenium (Se) on immunity attacked by exogenous active oxygen species, H2O2 and 60Co-radiation, respectively. Lipid peroxidation was also determined to observe the relation between antioxidation ability and protecting ability of Se. It was found that H2O2 injured lymphocytes immunocompetence deeply and 60Co-radiation decreased immune response capacity greatly, but that administration of Se counteracts this damage. The antioxidative ability of Se was correlated with its protecting ability.

Animals↗
PubMed1999

Effect of antioxidant supplementation on urine and blood markers of oxidative stress during extended moderate-altitude training.

OBJECTIVE: To investigate the increase in oxidative stress during work at moderate altitudes due to additional energy expenditure, tissue anoxia, and UV light exposure. METHODS: Thirty US Marine Corps volunteers were divided into placebo (P) and antioxidant supplement (S) groups and tested for markers of oxidative stress before (t0), at the midpoint of (t1), and after (t2) 14 days of winter training at a moderate altitude (approximately 2700 m). The antioxidant supplement consisted of a daily dose of 20,000 IU beta-carotene, 400 IU vitamin E, 500 mg vitamin C, 100 micrograms selenium, and 30 mg zinc. The following markers of oxidative stress were measured: urine thiobarbituric acid reactive substances (TBARSs), urine hydroxynonenal (HNE), urine 8-hydrodeoxyguanosine (8-OHdG), plasma total peroxyl radical trapping potential (TRAP), and plasma lipid hydroperoxides (LPOs). Urine was collected on a 24-hr basis at t0, t1, and t2; blood samples were collected at t0 and t2. RESULTS: P group LPOs increased 30% (p < 0.05) between t0 and t2, whereas S group LPOs did not increase. Both groups exhibited significant increases in urine TBARSs, HNE, and 8-OHdG by t2. Urine TBARSs, HNE, and 8-OHdG increased between t0 and t1 in both groups, with the greater increase in the S group. The conflicting results between the plasma and urine markers of oxidative stress may be due to a time-phase relationship. CONCLUSIONS: The results of this study suggest that work in a moderate-altitude cold-weather environment is accompanied by increased oxidative stress, despite relatively high intakes of dietary and supplemental antioxidants.

Adult↗
PubMed2005

Neurotransmitter level changes in domestic ducks (Shaoxing duck) growing up in typical mercury contaminated area in China.

The neurotransmitter level changes of ducks exposed 8-month in a mercury-polluted site (Wanshan, China) and a reference site (Shanghai, China) were examined. Chemical analyses showed both higher mercury and selenium concentrations in the organ of Wanshan ducks. An increased content of acetylcholine (ACh) in brain and blood and a decreased activity of acetylcholinesterase (AChE) in blood were observed. Moreover, there was an increasing trend for nitric oxide synthase (NOS) activity and nitric oxide(NO) production in duck brain, but a reduction of NOS activity in duck serum. The possible explanations were due to the interactive effect of selenium accumulation and the sublethal exposure level of mercury in Wanshan area. The present study showed that AChE and NOS were sensitive to mercury contamination of real circumstance, suggesting that these two indexes have the potential to be biomarkers in assessment of health effects by mercury contamination.

Acetylcholine↗
PubMed1995

[Selenium and antioxidant status in various diseases].

All healthy mammalian organisms are characterized by an equilibrium between the occurrence of highly reactive oxygen species and their destruction by anti-oxidants. Numerous diseases go hand in hand with a disturbance of the homoeostatis. In order to avoid or minimize the destructive effect of the oxidant stress on biological structures, therapies utilizing drugs with anti-oxidant effects are increasingly being applied. Preconditions for these therapies are a characterisation and a follow-up of the anti-oxidant status in the diseased organism. In the course of the present study selenium, glutathione peroxidase and malondialdehyde were determined in patients with various clinical pictures (terminal renal insufficiency, septic shock, high-risk gravidieties, arterioscleroisis, pulmonary carcinoma, acute myocardial infarction, test patients taking the contraceptive pill). Patients with terminal renal insufficiency and those suffering from septic shock syndromes clearly show a selenium decrease in serum and whole blood as well as a drop in the GSH-Px-activity, and increased malondialdehyde concentrations in the serum. Both are a reflection of an increased lipid peroxidation. First results of a selenium therapy are available for patients with therminal renal insufficiency and post-traumatically induced renal failure. The interpretation of the findings in the categories "high-risk gravidity" and "women on the contraceptive pill", which show a normal GSH-Px-activity and significantly increased malondialdehyde concentrations, seems problematic. The organism counteracts an increased lipid peroxidation with a normal plasma-GSH-Px-activity, clearly a sign of a still normal anti-oxidant potential.

Acute Kidney Injury↗
PubMed2002

The argument for increasing selenium intake.

The essential trace mineral, Se, is of fundamental importance to human health. As a constituent of selenoproteins it plays both structural and enzymic roles, in the latter context being best known as an antioxidant and catalyst for the production of active thyroid hormone. While Se-deficiency diseases have been recognised for some time, evidence is mounting that less-overt deficiency can also cause adverse health effects and furthermore, that supra-nutritional levels of Se may give additional protection from disease. In the context of these effects, low or diminishing Se status in some parts of the world, notably in some European countries such as the UK, is giving cause for concern. While deficiency has an adverse effect on immunocompetence, Se supplementation appears to enhance the immune response. Se appears to be a key nutrient in counteracting certain viral infections; thus, in a Se-deficient host the benign coxsackie virus becomes virulent, causing heart damage, the influenza virus causes more serious lung pathology and HIV infection progresses more rapidly to AIDS. Long recognised as essential for successful animal reproduction, Se is required for human sperm maturation and sperm motility and may reduce the risk of miscarriage. Deficiency has been linked to adverse mood states. Findings have been equivocal in linking Se to cardiovascular disease risk, although other conditions involving oxidative stress and inflammation have shown some association with Se status. There is growing evidence that higher Se intakes are associated with reduced cancer risk. While persuasive evidence already exists to suggest that additional Se would be beneficial in some health conditions, results from intervention trials underway or planned have the potential to reinforce or refute the argument for increasing Se intake.

Antioxidants↗
PubMed1997

The risk of developing lung cancer associated with antioxidants in the blood: ascorbic acid, carotenoids, alpha-tocopherol, selenium, and total peroxyl radical absorbing capacity.

Lung cancer cases diagnosed during the period 1975 through 1993 and matched controls were identified in the rosters of Washington County, Maryland residents who had donated blood for a serum bank in 1974 or 1989. Plasma from participants in the 1989 project was assayed for ascorbic acid; serum or plasma was assayed for participants in either project for alpha- and beta-carotene, cryptoxanthin, lutein/zeaxanthin, lycopene, alpha-tocopherol, selenium, and peroxyl radical absorption capacity. Among the total group of 258 cases and 515 controls, serum/plasma concentrations were significantly lower among cases than controls for cryptoxanthin, beta-carotene, and lutein/zeaxanthin with case-control differences of -25.5, -17.1, and -10.1%, respectively. Modest nonsignificant case-control differences in a protective direction were noted for alpha-carotene and ascorbic acid. There were only trivial differences for lycopene, alpha-tocopherol, selenium, and peroxyl radical absorption capacity. Findings are reported for males and females and for persons who had never smoked cigarettes, former smokers, and current smokers at baseline. These results and those from previous studies suggest that beta-carotene is a marker for some protective factor(s) against lung cancer; that cryptoxanthin, alpha-carotene, and ascorbic acid need to be investigated further as potentially protective factors or associates of a protective factor; and that lycopene, alpha-tocopherol, selenium, and peroxyl radical absorption capacity are unlikely to be associated with lung cancer risk. Until specific preventive factors are identified, the best protection against lung cancer is still the avoidance of airborne carcinogens, especially tobacco smoke; second best is the consumption of a diet rich in fruits and vegetables.

Adult↗
PubMed2004

[Effect of heavy metal ions on function of vascular endothelium in patients with ischemic heart disease].

UNLABELLED: Endothelium dysfunction is one of the first signs of atherosclerotic process. There are many factors known, which provoke such a dysfunction; many are still to be revealed. One of them may be a heavy metal ion. The aim of the study was to establish the link between heavy metal ions concentrations in blood and the endothelium dysfunction measured with the nitric oxide blood concentration in a population of patients with ischemic heart disease, not exposed occupationally to high concentrations of heavy metal ions. The study included 42 patients (24 men and 18 women, age 63.7 +/- 9.9 years) with angiography confirmed coronary artery disease. The study group was subdivided according to coronary artery atherosclerosis extent. Control included 18 patients (10 men and 8 women, age 58.7 +/- 9.4 years), where coronarography revealed no significant lesions in coronary arteries. In all persons blood for nitric oxide and heavy metal ions was collected. Heavy metal ions studied included: lead, copper, manganese, zinc, selenium, and cadmium. Heavy metal ions concentrations in studied and control group was within normal range for not exposed population and did not differ significantly with each other. No significant difference was observed between groups for nitric oxide concentration. Nitric oxide concentration correlated positively with zinc concentration in control group (p<0.001, Pearson r=0.70). Such a correlations was not present in studied group. After regression analysis there was still strong correlation between zinc and nitric oxide in control group (beta=0.43, p<0.01), the phenomenon not present in studied group. CONCLUSIONS: 1. In the group of patients with angiography confirmed ischemic heart disease heavy metal ions concentrations are within normal range for not exposed population and is not connected with coronary atherosclerosis extent. 2. From all heavy metal ions studied only zinc seams to have protective influence on endothelial function measured by nitric oxide production 3. No such a protective effect is observed in the group of patients with ischemic heart disease, which may be due to the relative zinc deficiency.

Adult↗
PubMedDate not supplied

Characterization and modulation by drugs of sheep liver microsomal flavin monooxygenase activity.

The flavin monooxygenases (FMO) catalyse the NADPH and oxygen-dependent oxidation of a wide range of nucleophilic nitrogen-, sulfur-, phosphorus-, and selenium heteroatom-containing chemicals, drugs, and agricultural agents. In the present study, sheep liver microsomal FMO activity was determined by measuring the S-oxidation rate of methimazole and the average specific activity obtained from different microsomal preparations was found to be 3.8 +/- 1.5 nmol methimazole oxidized min(-1) mg(-1) microsomal protein (mean +/- SE, n = 7). The presence of 0.1% Triton X-100 in the reaction mixture caused an increase of specific sheep liver microsomal FMO activity towards methimazole to 6.1 +/- 1.4 nmol methimazole oxidized min(-1) mg(-1) microsomal protein (mean +/- SE, n = 6). Metabolism of imipramine and chlorpromazine was measured by following the oxidation of cofactor NADPH spectrophotometrically at 340 nm. Sheep liver microsomal FMO activity towards imipramine and chlorpromazine was found to be 10.7 and 12.3 nmol NADPH oxidized min(-1) mg(-1) microsomal protein, respectively. Characterization of sheep liver enzyme was carried out using methimazole as substrate and the maximum FMO enzyme activity was detected at 37 degrees C and at pH 8.0. The apparent K(m) value of sheep liver microsomal FMO for methimazole was 0.118 mM. Effects of the detergents Triton X-100, Cholate, and Emulgen 913, on FMO activity were determined and FMO activity was found to increase with the addition of detergents to the reaction medium. Sheep liver microsomal FMO-catalysed methimazole oxidation was inhibited by imipramine and chlorpromazine when these drugs were used at high concentrations. Western blot-immunochemical analysis revealed the presence of FMO3 in sheep liver microsomes.

Animals↗