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Biomedical subjects

M Fields

Publications and source records attributed to M Fields.

At least 37 records · Page 2Linked to original sources
PubMed1996

Allopurinol, an inhibitor of xanthine oxidase, reduces uric acid levels and modifies the signs associated with copper deficiency in rats fed fructose.

This study was designed to focus on the potential stress that xanthine oxidase could produce in copper-deficient rats fed fructose. Fructose consumption results in an excess production of uric acid due to an increased degradation of nucleotides. The enzyme xanthine oxidase catalyzes the oxidation of both hypoxanthine and xanthine. During the oxidation process free radicals are generated, which in turn, induce lipid peroxidation and premature death. Allopurinol -- a competitive inhibitor of xanthine oxidase -- could alleviate the combined effects of fructose feeding and copper deficiency. Twenty-five male rats were fed for 4 weeks from weaning a copper-deficient or adequate diet containing fructose. Twelve rats were given a daily oral dose of 5 mg allopurinol/100 g b.wt. Two copper-deficient rats that were not treated with allopurinol died prematurely during the fourth week of the study. No mortality occurred in the group of copper-deficient rats that had been treated with allopurinol. Anemia was alleviated by allopurinol, which in turn, could be responsible for improved growth rate. Allopurinol was effective in inhibiting xanthine oxidase activity in vivo as measured by the dramatic reduction of uric acid production. Lipid peroxidation, however, was not affected by allopurinol. It is concluded that the beneficial effects of allopurinol in copper deficiency do not appear to be related to prevention of oxygen radicals, but rather, to the protection against the catabolic destruction of purines, which in turn, increases nucleotide pool.

Allopurinol↗
PubMed1996

Antioxidant defense system in lung of male and female rats: interactions with alcohol, copper, and type of dietary carbohydrate.

Male and female rats were used to investigate the effects of type of dietary carbohydrate (CHO), copper, and ethanol consumption on lung antioxidant enzyme activities and levels of phosphorylated compounds in whole blood. Copper-deficient female rats exhibited a greater degree of copper deficiency than males, as assessed by hepatic copper concentration and hepatic copper superoxide dismutase (CuSOD) activity. However, copper-deficient male rats fed fructose-containing diets exhibited greater growth retardation, anemia, and heart hypertrophy than females consuming the same diets and males fed starch. In addition, one of 10 copper-deficient male rats that ate a fructose-based diet and drank water and one of 10 copper-deficient male rats that ate a starch-based diet and drank ethanol died. Copper-deficient, starch-fed males exhibited the highest activities of glutathione peroxidase (GSH-Px) and catalase as compared with fructose-fed rats. Ethanol consumption elevated the activities of GSH-Px and catalase. Copper-deficient female rats exhibited higher catalase but lower GSH-Px activities than males. It is suggested that in copper deficiency, the ability to increase antioxidant enzyme activities in rats consuming starch is greater than in rats consuming fructose. Rats fed starch are provided with a greater degree of protection against oxidative damage than rats fed fructose. In addition, polyphosphorylated compounds in blood were reduced in copper-deficient male rats that consumed fructose-based diets. This may impair supply of oxygen to tissues.

Alcohol Drinking↗
PubMed1995

Dietary ferric vs. ferrous iron in copper-deficient rats fed fructose-based diets.

OBJECTIVE: This preliminary study was undertaken to determine whether the valence state of dietary iron affects signs associated with copper deficiency in rats fed fructose. METHODS: Rats were fed either copper-deficient or adequate diets containing 62% fructose as the sole dietary carbohydrate for 5 weeks. The mineral mixture contained equal concentration of either ferric or ferrous iron. RESULTS: Copper deficiency resulted in growth retardation, anemia, heart hypertrophy but pancreatic atrophy. The consumption of ferrous iron resulted in increased hematocrit and pancreas size. The combination of ferrous iron with copper deficiency reduced heart size. CONCLUSIONS: Copper deficiency had a major impact on each parameter measured. Although the valence state of iron did not protect the rats against the pathological consequence of copper deficiency it did have some positive effects. It may be that ferrous iron is a more available form than ferric iron.

Anemia↗
PubMed1995

Oxytocin and oxytocin receptor gene expression in the reproductive tract of the pregnant cow: rescue of luteal oxytocin production at term.

The peptide hormone oxytocin is produced both in the hypothalamus and in certain peripheral organs. The extent of extra-hypothalamic hormone synthesis in the pregnant cow has not previously been examined. In this study we have analyzed different tissues from the pregnant bovine reproductive tract and corpus luteum for the presence of mRNA encoding the oxytocin peptide as well as the oxytocin receptor. In uterine tissues oxytocin mRNA could only be detected sporadically with the help of a reverse transcription-polymerase chain reaction method, implying only very low levels of expression. The caruncles showed a consistently low level of oxytocin gene expression, which appeared up-regulated at term. However, in the corpus luteum there was a significant level of oxytocin gene expression at term, particularly following the onset of labor. The transcript levels were sufficiently high to be measurable by both RNase protection assay and by Northern hybridization; these levels imply a rescue of the oxytocin gene expression seen in the corpora lutea of cyclic and early pregnant cows. At the peptide level this expression was confirmed by immunohistochemistry. A sensitive RNase protection assay was developed to detect transcripts encoding the oxytocin receptor. Transcripts were detected in most uterine tissues, including the caruncles, with highest levels in the endometrium and myometrium at term. No transcripts could be detected in the corpus luteum at any stage of pregnancy, nor in the amnion. The results suggest the possibility of local, paracrine effects of oxytocin within the uterus of the pregnant cow. The rescue of luteal oxytocin at term could act to supplement the circulating hormone of pituitary origin.

Animals↗
PubMed1994

Coverage gaps in child-restraint and seat-belt laws affecting children.

Although most U.S. states have enacted mandatory-seat-belt-use laws and all states have child-restraint laws requiring children under specified ages to be properly restrained in vehicles, some children are covered by neither law. Other children are covered only by belt-use laws that do not make any adult responsible for their compliance. This note analyzes the child-restraint and belt-use laws in each state and demonstrates the deficiencies in coverage as they apply to children younger than age 16.

Adolescent↗
PubMed1994

Requirements for biotin are not affected by the combination of copper deficiency and fructose feeding.

OBJECTIVE: The objective of the present study was to establish whether copper (Cu)-deficient rats fed a diet containing fructose as their sole carbohydrate source require more biotin than the recommended 2 mg/kg diet when egg-white serves as the dietary protein. METHODS: Eighty weanling male Sprague-Dawley rats were randomly divided into 8 groups according to type of dietary carbohydrate (starch or fructose), level of Cu (0.6 micrograms Cu/g diet or 6.0 micrograms Cu/g diet) and level of biotin (2 mg/kg diet or 10 mg/kg diet). RESULTS: Regardless of the level of dietary biotin, Cu-deficient rats fed a fructose-containing diet exhibited growth retardation, anemia, atrophied pancreata, enlarged hearts and similar death rates. The remaining Cu-deficient rats fed fructose were emaciated and sick regardless of dietary biotin levels. The concentration of biotin in serum and biotin content of liver of rats fed fructose were higher than corresponding values from rats fed starch. CONCLUSION: Cu-deficient rats fed fructose are not deficient in biotin compared to published normal values. Supplementation of 10 mg/biotin/kg diet did not improve morbidity or mortality and therefore was not beneficial.

Animals↗
PubMed1993

Copper deficiency in rats: the effect of type of dietary protein.

The present investigation was conducted to determine whether type of dietary protein can exacerbate the pathology induced by the combination of fructose feeding and copper (Cu) deficiency. Weanling male Sprague-Dawley rats were assigned to three different groups differing in the nature of dietary protein. The proteins used were egg-white, casein or lactalbumin. All diets contained 62.5% carbohydrate as fructose and were low in Cu (0.6-0.72 microgram Cu/g diet). Although the lowest concentration of Cu was found in the livers of rats fed egg-white, the pathology associated with Cu deficiency was more severe in rats fed lactalbumin. The highest concentration of hepatic Cu was found in rats fed casein. The data show that the type of dietary protein can exacerbate signs associated with Cu deficiency. The concentrations of hepatic Cu do not reflect accurately the pathology associated with Cu deficiency.

Animals↗
PubMed1993

Low dietary iron prevents free radical formation and heart pathology of copper-deficient rats fed fructose.

Two studies were conducted to determine whether hepatic iron overload in rats fed fructose plays a role in the exacerbation of the signs associated with copper deficiency. When fed the adequate iron diet (50 micrograms Fe/g), copper-deficient rats fed either fructose or starch exhibited hepatic iron overload of similar magnitude. However, only livers of copper-deficient rats fed fructose exhibited the presence of high peaks associated with an iron compound detected by electron spin resonance. In addition, only copper-deficient rats fed fructose developed anemia, pancreatic atrophy, and heart hypertrophy with histopathologic changes, and they died prematurely of heart-related abnormalities. Lowering dietary iron from 50 micrograms/g to 30 micrograms/g was not sufficient to protect the animals against the pathologic consequences of copper deficiency. In contrast, the consumption of a fructose diet inadequate in both copper (0.6 micrograms/g) and iron (17 micrograms/g) resulted in the reduction of hepatic iron, which in turn caused the amelioration of the deficiency, compared with rats fed the adequate iron (50 micrograms/g) diet. None of these rats developed pancreatic atrophy, none exhibited myocardial lesions, and none died of the deficiency. Electron spin resonance spectra of their livers did not show the presence of free radicals. The data suggest that hepatic iron overload plays a role in the exacerbation of copper deficiency only when fructose diets are consumed.

Animals↗
PubMed1992

The effect of time of introduction of a high-fructose, low-copper diet on copper deficiency in male rats.

The purpose of the present study was to compare the time of introduction of the high-fructose low-copper diet on the expression of copper (Cu) deficiency. Weanling male rats were randomly assigned to either a diet containing 62.7% fructose or starch, and 6.0 (F+Cu) or 0.6 (S-Cu) microgram Cu/g diet, respectively, for either 1, 2, or 3 wk before being transferred to a diet containing fructose and inadequate in copper (F-Cu). At week 10, body weight and relative heart size of rats initially consuming the F + Cu diet was inversely related to the week placed on the F-Cu diet, but not for those initially consuming S-Cu. Hematocrit, hepatic Cu concentration and RBC superoxide dismutase activity were significantly lower in rats initially consuming S-Cu when compared to those fed F + Cu. Mortality was greatest in rats switched to the F-Cu diet at weeks 1 and 2 when compared to those switched at week 3 regardless of the type of diet initially consumed. Plasma cholesterol, triacylglycerols, and blood urea nitrogen concentrations were not significantly altered by the type of diet initially consumed or by the time of introduction of the F-Cu diet. It was concluded that changing rats to a F-Cu diet at 1, 2, or 3 wk after weaning did not significantly improve some of the characteristic signs associated with Cu deficiency, but the later that the F-Cu diet was introduced after weaning the greater the chances for survival.

Aging↗
PubMed1992

The influence of dietary carbohydrate and deferoxamine on developing copper deficiency of rats.

The present investigation was conducted to follow the development of copper deficiency in male rats from weaning (day 0) to day 31 of dietary copper deprivation and to correlate changes in tissue sizes with copper and iron concentrations. Male rats were fed for 31 days from weaning copper-deficient or adequate diets containing fructose or starch. Another copper-deficient group of rats that was fed fructose was treated with deferoxamine. Rats were killed at day 0, 8, 16, 24, and 31 of the study. In general, no correlation could be found between the development of heart hypertrophy, pancreatic and thymic atrophy, and tissue copper concentrations in copper-deficient rats fed fructose. In contrast, in the heart and pancreas a negative correlation existed between tissue size and iron concentration. In addition, anemia preceded heart hypertrophy. Deferoxamine lowered hepatic iron concentrations, ameliorated the anemia, and decreased heart size compared with untreated rats. The data of the present study suggest that tissue atrophy and hypertrophy and the severity of copper deficiency are not solely due to tissue concentrations of iron and/or copper.

Animals↗
PubMed1992

The influence of gender on developing copper deficiency and on free radical generation of rats fed a fructose diet.

The present investigation was conducted to determine whether differences in copper and iron status between male and female rats can be detected during the development of copper deficiency. These differences may explain the protection of the female against the severity of copper deficiency. In addition, the livers of all rats were exposed to electron-spin resonance (ESR) spectroscopy for the presence of free radicals. Male and female rats were fed from weaning either copper-deficient or -adequate diets containing fructose for 31 days. Rats were killed at day 0, 8, 16, 24, and 31 of the study. Throughout the study, copper-deficient males exhibited the same organ copper concentrations as copper-deficient female rats. However, only in the male did copper deficiency cause a reduction in body weight and an increase in liver and heart sizes but a decrease in pancreas size. In contrast, organ iron concentrations were different between males and females. Only copper-deficient males were anemic. Only the livers of copper-deficient males showed the presence of free radicals. Although the livers of copper-deficient female rats exhibited higher concentrations of hepatic iron than their male counterparts, their livers did not show the presence of free radicals. The data of the present study suggest that changes in organ sizes and the severity of copper deficiency are not solely due to the total concentrations of iron and/or copper. The type of iron compound and the presence of free radicals may be involved in the pathology of copper deficiency of the male.

Analysis of Variance↗
PubMed1992

Cardiomyopathy of copper deficiency: effect of vitamin E supplementation.

The present study was undertaken to determine whether the intraperitoneal injection of vitamin E to copper-(Cu) deficient rats fed fructose will protect the animals against the severity of Cu deficiency. Cu-deficient and adequate rats were fed a diet containing 62% carbohydrate as fructose. Half the Cu-deficient rats fed fructose were injected daily with vitamin E. Vitamin E treated rats were not protected against the lethal consequences of the interaction between Cu and fructose. These data provide evidence that the cardiomyopathy of Cu deficiency in rats consuming a fructose-based diet cannot be ameliorated by vitamin E supplementation.

Animals↗
PubMed1992

Garlic oil extract ameliorates the severity of copper deficiency.

This study was undertaken to determine whether a reduction in hepatic lipogenesis would be beneficial in the amelioration of copper (Cu) deficiency when fructose is fed. Garlic was chosen as the agent for reducing hepatic lipogenesis. Forty-eight weanling rats were fed Cu-deficient or adequate diets containing fructose or starch with or without garlic for 5 weeks. Garlic ameliorated the signs associated with Cu deficiency, although hepatic lipogenesis was not affected. Administration of garlic reduced the activity of the lipogenic enzyme glucose-6-phosphate dehydrogenase only in Cu-adequate rats. Consumption of garlic resulted in increased epididymal fat pad and pancrease sizes, and higher hematocrits, insulin and thyroxine concentrations. Mechanisms other than lipogenesis that could be responsible for this phenomenon are discussed.

Allyl Compounds↗
PubMed1992

Copper deficiency in rats: the effect of clofibrate.

This study was undertaken to determine whether hepatic lipogenesis plays a role in the exacerbation of copper (Cu) deficiency. Forty-eight male rats were fed from weaning a Cu-deficient or adequate diet containing 62% carbohydrate as either starch or fructose with or without clofibrate for 5 weeks. Clofibrate was fed since it had been shown to possess hypolipidemic properties. Administration of clofibrate reduced the activity of the lipogenic enzyme glucose-6-phosphate dehydrogenase. Total hepatic lipid, however, was not reduced. Clofibrate did not affect hepatic lipid concentration and the pathology associated with Cu deficiency when fructose was fed was not prevented by the consumption of clofibrate.

Animals↗