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Biomedical subjects

M Fields

Publications and source records attributed to M Fields.

At least 109 records · Page 6Linked to original sources
PubMed1975

The effect of beta aminoproprionitrile (BAPN) on experimental amyloidosis.

Experimental amyloidosis was induced in mice with repeated injections of complete Freund's adjuvant (CFA) reinforced with bacterial vaccine. BAPN administered in a mixture with CFA or on its own before the injection of CFA reduced the incidence of amyloidosis. The reduction in the incidence of amyloidosis following the administration of BAPN may be due to its inhibitory effect on the oxidative deamination of amino acids, which presumably inhibit cross-linking of amyloid fibrils or interfere with metabolic pathways which involve the formations of mucopolysaccharide formation. It is suggested that the defective formation of the mucopolysaccharide-amyloid protein complex inhibits amyloid deposition and induces the activity of beta glucuronidase observed in the present study. The reduced incidence of amyloidosis following BAPN adminsitration cannot be due to lysosomal enzyme degradation of the amyloid as the activity of cathepsin D and acid phosphatase is decreased during this process.

Acid Phosphatase↗
PubMedDate not supplied

X-ray microanalysis of isolated perfused rat hearts.

X-ray microanalysis was carried out on sections from isolated hearts perfused with a modified Krebs-Henseleit solution with or without isoproterenol. Changes in P, Ca and Zn concentrations could be detected after isoproterenol and some correlation with hemodynamic and morphological parameters was observed. Ratios between P/Ca in myonuclei and the ratios of interstitial cell to myofiber nucleus calcium were related directly to the state of the heart.

Animals↗
PubMedDate not supplied

Effect of coenzyme Q10 supplementation on cardiac hypertrophy of male rats consuming a high-fructose, low-copper diet.

Administration of coenzyme Q10 to humans and animals has a beneficial effect on a number of cardiac diseases. The purpose of the present study was to determine if coenzyme Q10 treatment could ameliorate cardiac abnormalities associated with the carbohydrate x copper interaction in rats. Weanling male rats were provided with a copper-deficient diet (0.6 microgram Cu/g) containing either 62.7% starch (S-Cu) or fructose (F-Cu) for 5 wk. Half of the rats provided with the F-Cu diet were given daily oral supplements of 300 mg coenzyme Q10/kg body weight (F-Cu + Q). Heart hypertrophy, liver enlargement, or pancreatic atrophy were not affected by, nor was body growth or anemia improved by, supplementation with coenzyme Q10 when compared to rats fed only the F-Cu diet. Hearts from rats fed the F-Cu diet had severe inflammation, degeneration, fibrosis, and giant mitochondria with abnormal cristae. Hearts from F-Cu + Q rats had similar mitochondrial changes as the F-Cu rat hearts but without any apparent degenerative changes. None of the F-Cu + Q rats, but 30% of the F-Cu rats, died during the study as a result of heart rupture. These observations show that whereas coenzyme Q10 treatment did not prevent the cardiac hypertrophy of the carbohydrate x copper interaction, it did play a role in maintaining the integrity of the heart.

Animals↗
PubMedDate not supplied

Dietary carbohydrate influences tissue fatty acid and lipid composition in the copper-deficient rat.

Fructose and copper have been shown independently to influence long chain fatty acid metabolism. Since fructose feeding exacerbates copper deficiency, their possible interaction with respect to tissue long chain fatty acid and lipid composition was studied. Weanling male Sprague-Dawley rats were given diets containing 0.6 or 6 mg/kg copper. The carbohydrate source (627 g/kg) was either fructose or corn starch. After 3 wk, fatty acid profiles and total lipids in heart and liver were analyzed. Copper-deficient rats fed fructose had more severe signs of copper deficiency than those fed starch, according to heart/body wt ratio, hematocrit, and liver copper content. The fatty acid composition of heart and liver triacylglycerol was significantly different between groups, but the changes did not correlate with the severity of copper deficiency. In heart, phosphatidylinositol and phosphatidylserine, arachidonic acid and docosapentaenoic acid (n-6) were increased 193 and 217%, respectively, p less than 0.05) in rats given the copper-deficient diet containing fructose. Changes in the long chain fatty acids in heart phospholipids may be related to the higher mortality commonly observed in rats fed a copper-deficient diet containing fructose.

Animals↗
PubMedDate not supplied

Copper deficiency in rats increases pancreatic enkephalin-containing peptides and insulin.

Free enkephalins (enk) and higher molecular weight enkephalin-containing peptides (enk-c-p) are present in the endocrine pancreas of rats, presumably in B cells. To determine whether these opioid peptides show dynamic alterations as insulin content of pancreas changes, we utilized a copper deficient rat model, in which the exocrine pancreas atrophies and the endocrine pancreas is "intact" and insulin (IRI) content increases. Dietary copper deficiency (-C) was produced in weanling male rats for 4 and 7 weeks. The deficient and copper supplemented (+C) groups were further subdivided to receive all dietary carbohydrate as either 62% fructose (F) or 62% starch (S). -CF rats showed the most severe deficiency. After 7 weeks, total units of pancreatic IRI in -CF were 7.5 +CF 2.1, -CS 7.9 and in +CS 2.8 (p less than 0.001). Pancreatic content of Met5- and Leu5-enk was measured in extracts which were purified on C-18 Seppaks with and without prior treatment with trypsin and carboxypeptidase B. -C animals showed progressive, significant increases in pancreatic content of Leu-enk-c-p, with a decrease in free Leu- and Met-enk (p less than 0.02-0.01). The pancreatic findings are compatible with a co-localization of enkephalins and insulin in the endocrine pancreas and are suggestive of co-regulation.

Animals↗
PubMedDate not supplied

Antioxidant defense mechanisms in the male rat: interaction with alcohol, copper, and type of dietary carbohydrate.

The activities of enzymes participating in cellular protection against free radical reactions were measured in hepatic tissues from copper-adequate and copper-deficient rats fed fructose or starch-based diets. Half of the rats consumed 20% ethanol in their drinking water. The consumption of ethanol depressed growth rate, reduced hematocrit, and hepatic copper concentration. Feed efficiency was greatly depressed by ethanol. Mortality due to copper deficiency occurred in fructose-fed rats and in starch-fed rats that drank ethanol. Ethanol had no effect on superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), or catalase. In contrast, copper deficiency reduced SOD and fructose feeding depressed catalase activity. GSH-Px was not affected by either the type of dietary carbohydrate, copper, or ethanol. Taken together, these data suggest that additional mechanisms to antioxidant defense systems are responsible for the metabolic changes that occur during the interactions between ethanol low copper and dietary carbohydrates.

Animals↗
PubMedDate not supplied

Antioxidant defense mechanisms in the female rat: interactions with alcohol, copper, and type of dietary carbohydrate.

The purpose of this study was to examine the effects of ethanol, type of dietary carbohydrate (fructose vs. starch), and levels of dietary copper (deficient vs. adequate) on antioxidant defense mechanism in the female rat. The consumption of 20% ethanol in the drinking water depressed growth rate due to a reduction of feed efficiency. Ethanol also lowered hepatic copper concentration, but had no effect on hepatic iron. Among the three antioxidant enzymes studied [i.e., superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase], only catalase activity was increased by ethanol. This effect was independent of copper or the type of dietary carbohydrate. As expected, copper deficiency dramatically reduced SOD. Copper deficiency also reduced GSH-Px activity; however, the combination of fructose feeding with copper deficiency caused a further reduction in GSH-Px. The data show that copper deficiency, per se, and the combination of copper deficiency with fructose feeding lower the antioxidant defense system in female rats.

Alcohol Drinking↗