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Biomedical subjects

W G Hoekstra

Publications and source records attributed to W G Hoekstra.

At least 37 records · Page 2Linked to original sources
PubMed1978

Metabolism of 35S-labelled copper-, zinc-and cadmium-thionein in the rat.

A comparative study has been made of the metabolism in the rat of intravenously-administered hepatic copper-, zinc- and cadmium-thioneins. In all cases the 35S-labelled protein was rapidly removed from the circulation. About 20% of the 35S was present in the kidneys after 30 min byt only small amounts of 35S were found in the liver, intestinal mucosa or pancreas. In the case of copper-thionein, 30% of the injected 35S was recovered in the urine within 2 h, mainly as intact copper-thionein. The 35S which appeared in the kidneys was also present initially as metallothionein but this was degraded very rapidly, especially when zinc-thionein was give. Both copper and cadmium from the injected proteins accumulated in the kidneys as metallothionein, but there was no increase in renal zinc concentrations in the rats dosed with zinc-thionein. These findings are discussed in relation to the development of renal damage in chronic cadmium and copper toxicity.

Animals↗
PubMed1977

Protection against carbon tetrachloride-induced lipid peroxidation in the rat by dietary vitamin E, selenium, and methionine as measured by ethane evolution.

Dietary vitamin E, selenium (Se), and methionine were tested for their ability to inhibit carbon tetrachloride (CCL4)-induced lipid peroxidation. Peroxidation, in vivo, was monitored by the evolution of ethane, an autoxidation product of omega-3-unsaturated fatty acids. Weanling rats were fed a basal diet low in vitamin E, Se, and sulfur-containing amino acids, or diets individually supplemented with these factors. After 3 to 7 weeks, the rats were injected with CCL4 (ip) and ethane was collected for 9 hours. Cumulative ethane evolution was increased by CCl4 in all groups. Vitamin E, Se, and methionine reduced ethane evolution from CCl4-treated rats by 82%, 74%, and 60%, respectively. The toxicity of CCl4 was decreased in correlation with ethane evolution. Thus, methionine and Se, probably by maintaining intracellular glutathione and glutathione peroxidase, protected against CCl4-induced lipid peroxidation, as did vitamin E. Substitution of cod liver oil, which is rich in omega-3-unsaturated fat, for lard in the basal diet increased CCl4-induced ethane evolution six-fold. Relative inhibition by the dietary supplements was not changed. Thus, the feeding of cod liver oil greatly increased ethane production which facilitated the detection and measurement of lipid peroxidation in vivo.

Animals↗
PubMed1977

Lipid peroxidation in vivo during vitamin E and selenium deficiency in the rat as monitored by ethane evolution.

Ethane evolution was monitored from vitamin E and selenium (Se)-deficient rats to determine if lipid peroxidation occurs in vivo when these rats develop fatal organ lesions. Weanling rats were fed a vitamin E and Se-deficient, or supplemented, diet for 40 to 90 days. Each was then prefasted for 4 hours and fasting was continued for 24 to 40 hours while ethane was collected. Approximately 50% of the doubly-deficient rats died as a result of fasting. Pathological signs included hematuria, lung hemorrhage, and liver necrosis. Ethane evolution increased exponentially 10 to 20 hours before death and then declined 2 hours before death. Rats that survived (at least 5 days after ethane collection) evolved 7.4+/-1.3 nmoles ethane/100 g body weight/24 hours compared to 100+/-6 for rats that died. Supplementation of the basal diet with vitamin E (200 IU/kg), Se (0.2 ppm, as Na2SeO3), or both, completely prevented mortality and reduced ethane evolution values to 0.4+/-0.2, 3.1+/-0.4, or 0.2+/-0.2, respectively. These experiments indicate that lipid peroxidation occurs in vivo as a result of vitamin E and Se deficiency, and the peroxidation process greatly accelerates during the terminal phase of the fatal disease.

Animals↗
PubMed1975

Alleviation of silver toxicity by selenite in the rat in relation to tissue glutathione peroxidase.

Dietary Se (0.5 ppm Se supplied as sodium selenite to a casein-based diet containing 0.02 ppm Se and lacking in vitamin E) prevented the growth depression observed in rats receiving 76 ppm Ag in the water supply and markedly improved growth and survival of those given 751 ppm Ag. The Ag concentration of liver and possibly of kidney was increased by Se. Liver glutathione peroxidase activities from rats fed 0.5 ppm Se and given 76 and 751 ppm Ag for 52 days in their water were, respectively, 30% and 4% of those from control rats fed 0.5 ppmSe without Ag. In rats fed a diet, adequate in vitamin E (100 IU/kg) and Se (0.5 ppm as sodium selenite), administration of 751 ppm Ag in the water for 15 wk reduced liver GSH-Px activity to 5% of that from control rats receiving no Ag. GSH-Px activity of erythrocytes and kidney was decreased by Ag to 37% and 38%, respectively, of control values. It is concluded that in vivo administration of Ag dramatically decreased liver GSH-Px in rats fed Se-supplemented diets with or without vitamin E. Furthermore, supplemental Se (0.5 ppm) prevented the growth depression and mortality caused by Ag in rats fed a diet lacking vitamin E, while increasing the Ag concentration of liver and kidney.

Animals↗
PubMed1975

Effects of prednisone on gastric secretion and development of stomach lesions in swine.

In pigs treated with various doses of prednisone, pathologic changes appeared in the glandular region of the stomach, mainly in the fundic area and rarely and less severely in the cardiac and pyloric mucosae. The characteristic lesion was hemorrhagic gastritis; this was associated with massive gastric hemorrhages in pigs given the larger doses of prednisone. Epithelial changes were found in the esophageal area, but there were no ulcers. In pigs with gastric fistulas, prednisone administered at dose levels of 10 mg/kg of body weight for 8 days produced a significant increase in the volume and the acidity of gastric secretion. Hexosamine output, but not concentration, increased significantly during the treatment period. Change in pepsin secretion was sit significant. Prednisone did not produce an immediate change in gastric secretion--there being a latent period lasting 1 to 2 days before marked changes were observed. After peak changes occurred (3rd or 4th day of treatment), acidity gradually decreased to pretreatment level toward the end of the treatment period. This indicates that although increased acidity may be involved in the development of lesions in the glandular region, other factors probably have a role also in the pathogenesis of steroid-induced stomach lesions in swine.

Animals↗
PubMed1975

Biochemical function of selenium and its relation to vitamin E.

Glutathione peroxidase (glutathione:H2O2 oxidoreductase, E.C. 1.11.1.9), isolated from ovine and bovine erythrocytes, has recently been shown to contain 4 selenium atoms per mole, an average of 1 Se per protein subunit of about 22,000 molecular weight. Selenium deficiency in the rat, chick and sheep causes dramatic decreases in the activity of this enzyme in the tissues, but certain sites such as liver are affected more than others. Decreases in glutathione peroxidase correlate with lesions caused by selenium deficiency and appear useful in diagnosing selenium deficiency. Glutathione peroxidase is an important enzyme in destroying H2O2 and organic hydroperoxides such as lipid hydroperoxides. It therefore guards against oxidative damage to the cell membranes and other oxidant-sensitive sites in the cell. While this selenium-dependent system destroys lipid hydroperoxides and other peroxides, vitamin E is believed to protect against oxidant damage to membranes by preventing the formation of lipid hydroperoxides. A scheme is proposed, based on oxidant damage and its prevention, which accounts for the interaction between selenium, vitamin E, unsaturated lipids, sulfur-containing amino acids, and cell damaging agents such as oxidant stressors and toxicants such as silver and tri-o-cresyl phosphate. The background for such a scheme is reviewed.

Animals↗
PubMed1975

Plasma concentrations of pepsinogen and corticosteroid in relation to gastric lesions in swine.

Plasma pepsinogen and plasma corticosteroid concentrations were found to be unrelated to the presence or severity of gastric lesions in swine. Mean plasma pepsinogen and corticosteroid concentrations were significantly different between collection periods, with significantly higher values occurring during cold weather. Seemingly, plasma pepsinogen and corticosteroid values are neither indicative of susceptibility to, nor of the presence of, gastric erosions or ulcers in swine. However, plasma pepsinogen concentration may be a potential indicator of stress.

Adrenal Cortex Hormones↗