Evidence for Altered Structure and Impaired Mitochondrial Electron Transport Function in Selenium Deficiency
TL;DR: Electron microscopic observations revealed structural changes such as loss of cristae with proliferative and degenerative changes of the mitochondria in Se deficiency and involvement of Se in maintaining structure and functional efficiency of mitochondria is evident from the present study.
Abstract: Selenium (Se) deficiency in the experimental models, Coturnix coturnix japonica and Corcyra cephalonica, resulted in impaired mitochondrial substrate oxidations and lowered thiol levels. Studies with respiratory inhibitors confirmed reduced mitochondrial electron transport enzyme activities, especially at cytochrome c oxidase (COX), the terminal segment. Enhanced mitochondrial lipid peroxidation in Se deficiency was more pronounced in the heart tissue of the quail compared to other tissues. Glutathione peroxidase (GSH-Px) activity toward H2O2 and cumene hydroperoxide were generally low in the insect muscle tissue and activity toward H2O2 was maximal in the quail heart mitochondria that was not very sensitive to Se status. Lowered COX activity in Se deficiency was more directly correlated with the increased level of lipid peroxidation than with the GSH-Px activity measured, suggestive of Se mediated protective mechanisms independent of GSH-Px. Electron microscopic observations revealed structural changes such as loss of cristae with proliferative and degenerative changes of the mitochondria in Se deficiency. Involvement of Se in maintaining structure and functional efficiency of mitochondria is evident from the present study.
Citations
More filters
TL;DR: There is sufficient evidence to support a large-scale trial of dietary micronutrient supplementation in HF, and Carnitine, co-enzyme Q10 and creatine supplementation have resulted in improved exercise capacity in patients with HF in some studies.
229 citations
TL;DR: An optimum intake of micronutrients could tune up metabolism and give a marked increase in health, particularly for the poor, elderly, and obese, at little cost.
106 citations
TL;DR: Selenium supplementation of gestating beef cows benefited cows and calves by increasing WBSe and GSH-Px and the use of seleno-yeast as a Se supplement compared to sodium selenite increased theWBSe of both cows and their calves without affecting the T4 to T3 conversion or IGF-1 concentrations.
Abstract: Over 2 years, 32 beef cows nursing calves in southwest Arkansas were randomly selected from a herd of 120 that were managed in six groups and were assigned to six 5.1-ha bermudagrass (Cynodon dactylon [L.] Pers.) pastures. Treatments were assigned to pastures (two pastures/treatment) and cows had ad libitum access to one of three free-choice minerals: (1) no supplemental selenium (Se), (2) 26 mg of supplemental Se from sodium selenite per kilogram, and (3) 26 mg of supplemental Se from seleno-yeast per kilogram (designed mineral intake = 113 g/cow daily). Data were analyzed using a mixed model; year and pasture were the random effects and treatment was the fixed effect. At the beginning of the calving and breeding seasons, cows supplemented with Se had greater (P < 0.01) whole blood Se concentration (WBSe) and glutathione peroxidase activities (GSH-Px) than cows receiving no supplemental Se; cows fed seleno-yeast had greater (P ≤ 0.05) WBSe than cows fed sodium selenite, but GSH-Px did not differ (P ≥ 0.25) between the two sources. At birth and near peak lactation (late May), calves from cows supplemented with Se had greater (P < 0.01) WBSe than calves from cows fed no Se and calves from cows fed seleno-yeast had greater (P ≤ 0.01) WBSe and GSH-Px than calves from cows fed sodium selenite. Thyroxine (T4), triiodothyronine (T3), and the T4:T3 ratio in calves did not differ among treatments (P ≥ 0.35). At birth, insulin-like growth factor 1 (IGF-1) was greater (P = 0.02) in calves nursing cows with no supplemental Se than in ones with supplemental Se; in calves nursing cows with supplemental sodium selenite, IGF-1 did not differ (P = 0.96) from ones offered supplemental seleno-yeast. Selenium supplementation of gestating beef cows benefited cows and calves by increasing WBSe and GSH-Px. The use of seleno-yeast as a Se supplement compared to sodium selenite increased the WBSe of both cows and their calves without affecting the T4 to T3 conversion or IGF-1 concentrations.
31 citations
Cites background from "Evidence for Altered Structure and ..."
...Also, Se deficiencies can inhibit the immunoglobulin G response [6], detoxification of certain toxins [7], and the efficiency of mitochondrial transport chain [8]....
[...]
01 Jan 1954
TL;DR: In this article, three distinct dietary factors have been identified as protective against necrotic liver degeneration, namely, cystine (2, lo), vitamin E (ll), and Factor 3 (12).
Abstract: Dietary necrotic liver degeneration is recognized now as a distinct disease entity; it is a deficiency of complex nature, which, so far, has been produced in rats (2, 3), mice (4), rabbits,’ and pigs (5, 6). The disease in rats is primarily characterized by acute massive necrosis of the liver which develops suddenly after an uneventful experimental period of several weeks duration. In most animals, the first attack of necrosis is fatal. Only 23 per cent of the animals dying from the disease show signs of earlier episodes of necrosis of the liver (7, 8). A detailed description and discussion of the various facets of this deficiency disease are found in the monograph on “Nutritional factors and liver diseases” (9). Three distinct dietary factors have been identified as protective against necrotic liver degeneration, namely, cystine (2, lo), vitamin E (ll), and Factor 3 (12). Any one of these three chemically different substances affords protection by itself (10). Assuming that the acute attack of massive necrosis is the end-result of a degeneration of metabolism in the hepatic parenchyma, we have investigated in vitro the metabolism of tissues of rats on diets which produce liver necrosis. Slices from livers of such animals exhibit a peculiar metabolic lesion several weeks before hepatic necrosis appears. They are incapable of maintaining normal respiratory activity in the Warburg apparatus; oxygen consumption declines after 30 to 60 minutes at initially normal rates. In the following, this metabolic lesion is described, its relation to the three factors which specifically prevent dietary liver necrosis is demonstrated, its biochemical nature is partially defined, and it is compared to other experimentally induced types of hepatic damage.
27 citations
TL;DR: Selenium accumulates in gastric tissue when it is needed, as is the case in HP-related antral inflammation, and seems to disappear in the presence of precancerous gastric lesions in the setting of HP-associated gastritis.
Abstract: GOALS We investigated plasma and gastric mucosal selenium levels in patients with Helicobacter pylori (HP)-associated histopathologic findings in their gastric antral mucosa. STUDY Before and after a successful HP eradication therapy, we quantitated the plasma and antral selenium levels in patients with HP-associated chronic antral gastritis using atomic absorption flame emission spectrometry. The same measurements were done in patients with dyspeptic complaints who had normal antral histology and negative urease test. RESULTS Thirty-four patients were studied, of whom 24 had HP-associated chronic antral gastritis confirmed by histology and positive urease test; the control group included 10 healthy patients. There was no difference between the groups with regard to age, gender, and number of smokers. All patients with HP infection were diagnosed with diffuse antral gastritis. Histopathology showed that 11 (49%) had some degree of atrophy. Of the 11 patients, 7 were classified as having chronic atrophic gastritis (CAG) without intestinal metaplasia (IM), 4 had IM, and none had dysplasia. The plasma concentrations of selenium were found to be very similar in controls and HP-infected subjects (68.0 +/- 25.97 microg/L and 71 +/- 32.9 microg/L, respectively; p > 0.05). The antral biopsy samples of the patients with HP-associated gastritis contained significantly higher levels of tissue selenium than the controls (20.17 +/- 19.74 microg/g and 2.83 +/- 1.42 microg/g, respectively; p < 0.05). Also, it was shown that antral tissue selenium levels decrease after successful HP eradication therapy (20.17 +/- 19.4 microg/g and 7.4 +/- 4.56 microg/g, respectively; t < 0.05). The patients with HP gastritis were assigned to mild, moderate, and severe gastritis groups, according to the histopathologic degree of inflammation present. The antral gastric selenium levels were significantly higher in patients with moderate and severe HP gastritis (21.13 +/- 22.5 microg/g and 22.81 +/- 17.35 microg/g, respectively) than in patients with mild gastric inflammation (9.53 +/- 10.3 microg/g; p < 0.05). The selenium concentrations in the biopsies of patients with CAG were significantly lower than in those with HP gastritis who did not have CAG (9.45 +/- 6.44 microg/g vs. 19.13 +/- 22.48 microg/g, respectively; p < 0.05). CONCLUSIONS Selenium accumulates in gastric tissue when it is needed, as is the case in HP-related antral inflammation. This reactive increase in gastric mucosal selenium seems to disappear in the presence of precancerous gastric lesions in the setting of HP-associated gastritis.
27 citations
References
More filters
TL;DR: A water-soluble (at pH 8) aromatic disulfide [5,5′-dithiobis(2-nitrobenzoic acid] has been synthesized and shown to be useful for determination of sulfhydryl groups.
23,232 citations
TL;DR: This chapter discusses microsomal lipid peroxidation, a complex process known to occur in both plants and animals that involves the formation and propagation of lipid radicals, the uptake of oxygen, a rearrangement of the double bonds in unsaturated lipids, and the eventual destruction of membrane lipids.
Abstract: Publisher Summary This chapter discusses microsomal lipid peroxidation Lipid peroxidation is a complex process known to occur in both plants and animals It involves the formation and propagation of lipid radicals, the uptake of oxygen, a rearrangement of the double bonds in unsaturated lipids, and the eventual destruction of membrane lipids, producing a variety of breakdown products, including alcohols, ketones, aldehydes, and ethers Biological membranes are often rich in unsaturated fatty acids and bathed in an oxygen-rich, metal-containing fluid Lipid peroxidation begins with the abstraction of a hydrogen atom from an unsaturated fatty acid, resulting in the formation of a lipid radical The formation of lipid endoperoxides in unsaturated fatty acids containing at least 3 methylene interrupted double bonds can lead to the formation of malondialdehyde as a breakdown product Nonenzymic peroxidation of microsomal membranes also occurs and is probably mediated in part by endogenous hemoproteins and transition metals The direct measurement of lipid hydroperoxides has an advantage over the thiobarbituric acid assay in that it permits a more accurate comparison of lipid peroxide levels in dissimilar lipid membranes
11,945 citations
TL;DR: Two peaks of glutathione peroxidase activity were present in the Sephadex G-150 gel filtration chromatogram of rat liver supernatant when 1.5 mM cumene hydroperoxide was used as substrate, and the second peak represents a second glutathienase activity which catalyzes the destruction of organic hydroperoxides but has little activity toward H 2 O 2 and which persists in severe selenium deficiency.
3,181 citations
392 citations