Ingo H. Waschulewski

Bio: Ingo H. Waschulewski is an academic researcher from University of Arizona. The author has contributed to research in topics: Methionine & Glutathione peroxidase. The author has an hindex of 2, co-authored 2 publications receiving 163 citations.

Effect of dietary methionine on utilization of tissue selenium from dietary selenomethionine for glutathione peroxidase in the rat.

Abstract: To study the effect of dietary methionine on the bioavailability of Se from selenomethionine ([Se]Met), weanling rats were first loaded with Se by feeding 05 mg Se as [Se]Met per kg diet of a low methionine (017% by analysis) torula yeast-based diet for 21 d, and then were fed an Se-deficient diet (less than 002 mg Se/kg) supplemented with 0, 04 or 09% methionine for 28 d Plasma, liver and muscle Se increased 26-, 25- and 22-fold, respectively, during [Se]Met supplementation, and then the tissue Se declined exponentially during the Se-deficient diet period Plasma, liver and muscle glutathione peroxidase (GSH-Px) activities decreased 43-50% during the [Se]Met supplementation period in spite of the increase in tissue Se When these [Se]Met-loaded rats were fed the Se-deficient diet and supplemented with methionine, tissue GSH-Px activities increased significantly within 3 to 7 d, but then decreased for the remainder of the experiment Calculation of the percentage of tissue Se present as Se in GSH-Px indicated that substantial Se from dietary [Se]Met was stored in tissues in a form different from GSH-Px when a low methionine diet was fed These results indicate that the dietary methionine level can modulate the availability of Se from dietary [Se]Met and from stored tissue [Se]Met; the inability of stored [Se]Met to provide Se for GSH-Px synthesis over a prolonged period of time suggests that [Se]Met may not be an optimum form for Se supplementation

Effect of dietary methionine on tissue selenium and glutathione peroxidase (EC 1.11.1.9) activity in rats given selenomethionine

Abstract: 1. The effect of dietary methionine on the utilization of selenium from dietary selenomethionine [( Se]Met) for tissue Se deposition and for glutathione peroxidase (EC 1.11.1.9; GSH-Px) synthesis was studied in male weanling rats. 2. When rats were given 0.5 mg Se as [Se]Met/kg diet supplemented with 0, 4 or 9 g methionine/kg, Se in plasma, erythrocytes, liver and muscle increased significantly over the 20 d period for all methionine-treatment groups. The increases in erythrocyte and muscle Se, however, were significantly higher in rats fed on the methionine-deficient diet compared with the methionine-supplemented diets. 3. In contrast to the increases in tissue Se, GSH-Px activity in liver, plasma and muscle decreased in methionine-deficient rats given 0.5 mg Se as [Se]Met/kg whereas GSH-Px activity was maintained or increased in rats supplemented with methionine. 4. The percentage of tissue Se associated with GSH-Px was calculated from the measured Se concentration and GSH-Px activity. A significantly lower percentage of Se was associated with GSH-Px in methionine-deficient rats compared with methionine-supplemented rats. 5. These results show that Se from dietary [Se]Met is preferentially incorporated into body proteins rather than used for GSH-Px synthesis when methionine is limiting in the diet. 6. These results further suggest that [Se]Met might not be the optimum Se compound to use for Se supplementation because metabolism of dietary [Se]Met to a biochemically active form, such as GSH-Px, was impaired when [Se]Met was provided in diets low in methionine.

The antioxidant role of selenium and seleno-compounds

Abstract: Selenium (Se) is an essential trace element for animals and humans that is obtained from dietary sources including cereals, grains and vegetables. The Se content of plants varies considerably according to its concentration in soil. Plants convert Se mainly into Se-methionine (Se-Met) and incorporate it into protein in place of methionine (Met). Selenocystine (Se-Cys), methyl-Se-Cys and gamma-glutamyl-Se-methyl-Cys are not significantly incorporated into plant protein and are at relatively low levels irrespective of soil Se content. Higher animals are unable to synthesize Se-Met and only Se-Cys was detected in rats supplemented with Se as selenite. Renal regulation is the mode by which whole body Se is controlled. Se is concentrated in hair and nail and it occurs almost exclusively in organic compounds. The potentiating effect of Se deficiency on lipid peroxidation is enhanced in some tissues by concurrent deficiency of copper or manganese. In the in vitro system, the chemical form of Se is an important factor in eliciting cellular responses. Although the cytotoxic mechanisms of selenite and other redoxing Se compounds are still unclear, it has been suggested that they derive from their ability to catalyze the oxidation of thiols and to produce superoxide simultaneously. Selenite-induced cytotoxicity and apoptosis in human carcinoma cells can be inhibited with copper (CuSO(4)) as an antioxidant. High doses of selenite result in induction of 8-hydroxydeoxyguanosine (8-OHdG) in mouse skin cell DNA and in primary human keratinocytes. It may cause DNA fragmentation and decreased DNA synthesis, cell growth inhibition, DNA synthesis, blockade of the cell cycle at the S/G(2)-M phase and cell death by necrosis. In contrast, in cells treated with methylselenocyanate or Se methylselenocysteine, the cell cycle progression was blocked at the G(1) phase and cell death was predominantly induced by apoptosis.

Selenomethionine: A Review of Its Nutritional Significance, Metabolism and Toxicity

Abstract: Although the need for selenium in human and animal nutrition is well recognized, the question concerning the proper form of selenium for supplemental use is still being debated. Ideally, selenium should be supplemented in the form in which it occurs naturally in foods. Because the L-isomer of selenomethionine (Se-met) is a major natural food-form of selenium, synthetic L-Se-met or enriched food sources thereof such as selenium yeast are appropriate supplemental forms of Se for humans; for animals, DL-Se-met is acceptable. Ingested Se-met is either metabolized directly to reactive forms of selenium or stored in place of methionine in body proteins. Se-met metabolism is closely linked to protein turnover. At constant intakes in the nutritional range, tissue Se levels increase until a steady state is established, preventing the build-up to toxic levels.

Elemental selenium at nano size possesses lower toxicity without compromising the fundamental effect on selenoenzymes: comparison with selenomethionine in mice

Abstract: Glutathione peroxidase and thioredoxin reductase are major selenoenzymes through which selenium exerts powerful antioxidant effects. Selenium also elicits pro-oxidant effects at toxic levels. The antioxidant and pro-oxidant effects, or bioavailability and toxicity, of selenium depend on its chemical form. Selenomethionine is considered to be the most appropriate supplemental form due to its excellent bioavailability and lower toxicity compared to various selenium compounds. The present studies reveal that, compared with selenomethionine, elemental selenium at nano size (Nano-Se) possesses equal efficacy in increasing the activities of glutathione peroxidase and thioredoxin reductase but has much lower toxicity as indicated by median lethal dose, acute liver injury, and short-term toxicity. Our results suggest that Nano-Se can serve as an antioxidant with reduced risk of selenium toxicity.

Selenium and its relationship to cancer: an update.

Abstract: Selenomethionine (Semet) is the major seleno-compound in cereal grains and enriched yeast whereas Se-methylselenocysteine (SeMCYS) is the major seleno-compound in Se-accumulator plants and some plants of economic importance such as garlic and broccoli exposed to excess Se. Animals can metabolize both Semet and SeMCYS. Epidemiological studies have indicated an inverse relationship between Se intake and the incidence of certain cancers. Blood or plasma levels of Se are usually lower in patients with cancer than those without this disorder, but inconsistent results have been found with toenail-Se values and the incidence of cancer. There have been eight trials with human subjects conducted on the influence of Se on cancer incidence or biomarkers, and except for one, all have shown a positive benefit of Se on cancer reduction or biomarkers of this disorder. This is consistent with about 100 small-animal studies where Se has been shown to reduce the incidence of tumours in most of these trials. Se-enriched yeast is the major form of Se used in trials with human subjects. In the mammary-tumour model, SeMCYS has been shown to be the most effective seleno-compound identified so far in reduction of tumours. Several mechanisms have been proposed on the mechanism whereby Se reduces tumours. Even though SeMCYS was shown to be the most effective seleno-compound in the reduction of mammary tumours, it may not be the most effective seleno-compound for reduction of colon tumours.

Selenocompounds in Plants and Animals and their Biological Significance

Abstract: There are several selenocompounds in tissues of plants and animals. Selenate is the major inorganic selenocompound found in both animal and plant tissues. Selenocysteine is the predominant selenoamino acid in tissues when inorganic selenium is given to animals. Selenomethionine is the major selenocompound found initially in animals given this selenoamino acid, but is converted with time afterwards to selenocysteine. Selenomethionine is the major selenocompound in cereal grains, grassland legumes and soybeans. Selenomethionine can also be the major selenocompound in selenium enriched yeast, but the amount can vary markedly depending upon the growth conditions. Se-methylselenocysteine is the major selenocompound in selenium enriched plants such as garlic, onions, broccoli florets and sprouts, and wild leeks.