Search PubMed⌕ Search

Biomedical subjects

J D Bogden

Publications and source records attributed to J D Bogden.

At least 37 records · Page 2Linked to original sources
PubMed1992

Dietary calcium modifies concentrations of lead and other metals and renal calbindin in rats.

We studied the effects of dietary calcium on kidney, femur, testis, liver, heart and brain concentrations of lead, magnesium, iron, copper, calcium and zinc in rats exposed to lead for 1 y. Renal levels of the 28,000 Da, vitamin D-dependent, calcium-binding protein calbindin-D28K were also measured. Seventy-two weanling male Sprague-Dawley rats were randomly assigned to one of nine treatment groups. Rats were fed diets containing 0.1, 0.5 or 2.5% Ca for 52 wk and were simultaneously given either 0, 50 or 100 mg lead/L in their drinking water. Rats fed the 0.1% Ca diet had organ lead concentrations that were two- to 20-fold greater than the corresponding animals fed 0.5% Ca. Rats fed diets containing 2.5% Ca had the lowest organ lead concentrations. Despite substantial effects of diet Ca on organ lead concentrations, Ca did not significantly influence concentrations of most other divalent metals studied with the exception of kidney calcium and magnesium, testis iron, plasma ionic calcium and magnesium, and several femur metals. Kidney calcium concentrations were lower in rats fed 2.5% Ca diets than in those fed 0.1 or 0.5% Ca diets. For rats not given lead, renal calbindin concentrations were highest in rats fed 0.1% Ca, and lowest in rats fed 2.5% Ca. Lead inhibited an increase in renal calbindin in the rats fed 0.1% Ca, but paradoxically increased renal calbindin levels in animals fed 2.5% Ca.

Administration, Oral↗
PubMed1992

Effects of essential hypertension and antihypertensive medications on sweat formation.

OBJECTIVE: Sweat volume and ionic composition depend to a large extent upon the cytosolic free calcium level in secretory sweat cells and sodium and potassium transport in the reabsorptive sweat duct. Since essential hypertension and its treatment with antihypertensive drugs is likely to be associated with altered cellular ionic regulation, the objective of this research was to explore sweat formation and sweat parameters in hypertensive and normotensive subjects. DESIGN: Black and white hypertensive and normotensive subjects of both genders were studied. Essential hypertensives were on or off antihypertensive medication. METHODS: Pilocarpine iontophoresis was used to induce sweat in a 5-cm2 area of the middle forearm. Sweat was analyzed for volume, sodium and potassium concentrations. RESULTS: Females demonstrated lower sweat volumes after pilocarpine stimulation than males. Untreated hypertensive white males exhibited a higher pilocarpine-induced sweat volume and sweat sodium excretion than normotensive white males, whilst hypertensive white males on antihypertensive medication showed a lower sweat volume and sweat sodium excretion than both normotensive white males and untreated essential hypertensive white males. Although untreated hypertensive white females did not show significant alterations in sweat parameters, treated hypertensive white females exhibited lower sweat volume and sweat sodium excretion than both the normotensive and untreated essential hypertensive white females. These hypertension and drug related alterations were not present in hypertensive black males and females. CONCLUSIONS: The results are consistent with the heterogeneous nature of essential hypertension and the diversity of the response to antihypertensive therapy. They suggest that the effect of antihypertensive medication on sweat formation is mediated through cytosolic free calcium.

Adult↗
PubMed1991

Dietary lead and calcium: effects on blood pressure and renal neoplasia in Wistar rats.

We examined the potential of increased Ca in the diet to modify the effects of Pb on tissue metal concentrations, blood pressure and the incidence of renal tumours. We randomly assigned 48, 5-wk-old male Wistar rats to one of six treatment groups. They were fed a low (0.2%) or high (4.0%) Ca diet for 31 wk and given 0, 1.0 or 100 micrograms Pb/mL in drinking water. In the low Ca groups, increasing concentrations of Pb produced graded increases in mean blood pressure. Rats receiving 4.0% Ca had higher mean blood pressures than the animals fed the 0.2% Ca diet. The 4.0% Ca diet also caused renal and urinary bladder stones to develop in some rats. The high Ca diet did not prevent dose-dependent increases in tissue Pb accumulation, but it caused significant decreases in kidney Cu, femur Mg and Fe in kidney, liver and testis. Femur Mg and Fe and liver Fe concentrations were lowest in rats receiving 4.0% Ca and 100 micrograms Pb/mL. Precancerous and cancerous renal lesions occurred to the greatest extent in the rats receiving 100 micrograms Pb/mL and the high Ca diet. These results suggest that high dietary Ca does not protect against Pb-induced increases in blood pressure or Pb accumulation in tissues and may often produce nephrocalcinosis. In addition, high dietary Ca in the presence of Pb may increase the incidence of renal tumors.

Animals↗
PubMed1990

Effects of one year of supplementation with zinc and other micronutrients on cellular immunity in the elderly.

The objective of this study was to determine the effects of a year of Zn supplementation on Zn concentrations in circulating cells and on cellular immune functions in the elderly. Subjects, aged 60-89, were given a placebo, 15 mg Zn, or 100 mg Zn daily for 12 months. All subjects also received a multivitamin/mineral supplement that contained no additional Zn. Blood samples were drawn and immune functions assessed prior to and at 3, 6, 12, and 16 months after beginning Zn supplementation. Subject diets were also assessed at each visit. Dietary folate, pyridoxine, alpha-tocopherol, copper, zinc, and magnesium were consistently below recommended intakes. Although plasma Zn increased significantly in the 100 mg Zn treatment group, concentrations of Zn in erythrocytes, mononuclear cells, polymorphonuclear leukocytes, and platelets were not significantly increased by zinc supplementation. Natural killer cell activity was transiently enhanced by the 100 mg/day dose of Zn. There was a progressive improvement in delayed dermal hypersensitivity (DDH) and in lymphocyte proliferative responses to two mitogens; this may have been due to one or more components of the multivitamin/mineral supplement administered to all study subjects. The enhancement of DDH was significantly greater in the placebo group than in either zinc treatment group. Thus, zinc had a beneficial effect on one measure of cellular immune function while simultaneously having an adverse effect on another measure of cellular immunity.

Aged↗
PubMed1990

Effect of zinc-deficient diet of varying duration on intestinal disaccharidase activity in the rat.

To determine whether zinc has a specific role on weight gain and intestinal disaccharidase activity, 42 male Sprague-Dawley rats were assigned to one of seven groups (n = 6 each). These were a baseline control group (0) that was killed to analyze initial intestinal disaccharidase (sucrase and maltase) activity, a second group (A) fed a zinc-deficient diet for 1 week, a third group (B) pair-fed control for A, a fourth group (C) fed a zinc-deficient diet for 2 weeks, a fifth group (D) pair-fed control for C, a sixth group (E) fed a zinc-deficient diet for 3 weeks, and a seventh group (F) pair-fed control for E. All experimental groups received distilled deionized drinking water, whereas control groups received zinc-enriched (25 micrograms of zinc/ml) distilled deionized water. Water was given ad libitum. After killing, the mucosa of the proximal half of the small intestine was analyzed for protein and disaccharidase activity, and liver, kidney, and heart were analyzed for zinc concentration. Protein content and disaccharidase activity of the jejunal mucosa in the experiment and control groups did not differ significantly. However, animals on the zinc-deficient diet demonstrated mildly depressed growth rates that were proportional to the duration of the experiment, and significantly lower zinc concentration in the kidney in the experimental groups. The data indicate that administration of a zinc-deficient diet for up to 3 weeks did not result in significant changes in intestinal mucosa protein content or in disaccharidase activity.

Animals↗
PubMed1990

Micronutrient status and human immunodeficiency virus (HIV) infection.

This study surveyed serum concentrations of vitamins, electrolytes, and trace elements in subjects seropositive for HIV-1 by ELISA and confirmatory Western blot. Thirty subjects (26 males, 4 females) were recruited at a hospital clinic. Seventeen were classified as having mild or severe ARC (AIDS-related complex), 7 had AIDS, and 6 were asymptomatic. Eight had experienced weight loss of 10 pounds or more in the past 6 months. Most (93%) were anergic to skin test antigens. Percentages of subjects with below normal plasma concentrations include: zinc-30%, calcium-27%, magnesium-30%, carotenes-31%, total choline-50%, and ascorbate-27%. Eighty-seven percent of the subjects had at least one abnormally low value. Percentages with above normal values include: folate-37% and carnitine-37%. Some subjects with above normal values for plasma vitamins reported self-supplementation, usually with large doses. The results suggest that one or more abnormally low concentrations of the plasma micronutrients studied here are likely to be present in the majority of HIV seropositive patients.

AIDS-Related Complex↗
PubMed1989

Reducing bone lead content by chelation treatment in chronic lead poisoning: an in vivo X-ray fluorescence and bone biopsy study.

A stained-glass artist with longstanding exposure to lead presented with neuropsychiatric symptoms. He was evaluated before and after chelation treatment by the CaNa2 EDTA lead mobilization test, iliac crest bone lead measurement, and in vivo tibial X-ray fluorescence (XRF). The three methods showed a progressive fall in body lead stores during chelation therapy in association with improvement in symptoms and a fall in blood lead and zinc protoporphyrin levels. In vivo tibial XRF is a safe, rapid, and noninvasive technique for detecting excessive body lead burdens. XRF measurement of bone lead content is a practical method for monitoring the efficacy of therapy as well as for establishing the diagnosis.

Biopsy↗
PubMed1988

Zinc and immunocompetence in elderly people: effects of zinc supplementation for 3 months.

One hundred and three apparently healthy elderly subjects age 60-89 y were randomly assigned to one of three treatments: placebo, 15 mg zinc/d, or 100 mg Zn/d for 3 mo. Plasma Zn was significantly increased only in the 100 mg Zn group. Zn concentrations in erythrocytes, platelets, mononuclear cells, and polymorphonuclear leukocytes were not significantly increased by any treatment. None of the treatments significantly altered delayed dermal hypersensitivity (DDH) to a panel of seven recall antigens or in vitro lymphocyte proliferative responses (LPR) to mitogens and antigens. Fifteen subjects had initially poor lymphocyte proliferative responses that improved in 14 of these individuals during the study; this was not due to Zn supplementation but might have been caused by one or more components of a vitamin-mineral supplement administered to all study subjects.

Aged↗
PubMed1987

Zinc and immunocompetence in the elderly: baseline data on zinc nutriture and immunity in unsupplemented subjects.

Zinc nutriture and immune function were studied in 100 subjects, age 60-89 yr. Mean (+/- SD) zinc concentrations found were 84.8 +/- 15.5 micrograms/dL (13.0 +/- 2.4 microM) for plasma, 1.04 +/- 0.24 micrograms (0.016 +/- 0.004 mumol)/10(9) cells for erythrocytes, 4.06 +/- 1.85 micrograms (0.062 +/- 0.028 mumol)/10(9) cells for mononuclear cells, 3.91 +/- 1.77 micrograms (0.060 +/- 0.027 mumol)/10(9) cells for polymorphonuclear leukocytes, 0.53 +/- 0.39 micrograms (0.0081 +/- 0.0060 mumol)/10(9) cells for platelets, and 222 +/- 101 micrograms (3.39 +/- 1.54 mumol)/g for hair. Zinc ingestion was below the RDA in more than 90% of study subjects. The incidence of anergy to a panel of seven skin test antigens was 41%; responses to these antigens were significantly associated with the plasma zinc concentration. Subjects with depressed lymphocyte responses to mitogens had significantly lower platelet and significantly higher mononuclear cell zinc concentrations than those with normal responses.

Aged↗
PubMed1987

Effect of cimetidine on tissue distribution of some trace elements and minerals in the rat.

Cimetidine is a histamine H2-receptor antagonist that is used in the treatment of patients with gastric and duodenal ulcers and other hypersecretory conditions. This drug has a structure that suggests that it could act as a chelating agent. To examine its effects on trace metal and mineral metabolism, 38 weanling male Sprague-Dawley rats were assigned to one of five treatment groups. These were a high dose [(HD) 1750 mg/(kg X d)] group, HD pair-fed control (HDPF) group, intermediate dose [(ID) 875 mg/(kg X d)] group, ID pair-fed (IDPF) group and low dose [(LD) 87.5 mg/kg X d)] group. In a separate experiment, 20 female Sprague-Dawley rats were assigned to one of two treatment groups: a high dose cimetidine group [(HDFem) 1750 mg/kg X d)] and a pair-fed control group (PFFem). Cimetidine was administered intragastrically four times per week for 5 wk. Significant differences (P less than 0.05) found among groups for the male rats studied included higher plasma copper in the HD and the ID groups, higher plasma sodium, liver copper, heart calcium and heart zinc in the HD group and a lower percentage of fecal excretion of all the divalent metals studied in the HD and the ID groups than in their pair-fed controls. Pathologic examination of the liver revealed extensive fatty infiltration of liver cells, liver cell necrosis and disrupture of liver lobular architecture in the HD group. Cimetidine-dosed females had higher zinc in heart and plasma, higher copper in heart, kidney, liver, jejunum, ileum and uterus, higher manganese in stomach and ileum, lower iron in kidney and liver, lower kidney calcium and higher stomach calcium and lower liver magnesium compared with their pair-fed controls. Levels of liver and kidney metallothionein in the two groups were comparable. Male and female rats receiving high dose cimetidine experienced significant changes in tissue concentrations of some of the trace metals and minerals studied.

Animals↗
PubMed1986

Effect of selenium and molybdenum on methylbenzylnitrosamine-induced esophageal lesions and tissue trace metals in the rat.

Thirty-six weanling male Sprague-Dawley rats were randomly assigned to one of four treatment groups: SE rats received 4.0 ppm selenium as sodium selenite in drinking water containing 1% sucrose; 15MO rats received 15 ppm molybdenum as sodium molybdate in the drinking water; 45MO rats received 45 ppm molybdenum in their water; and CON rats received distilled-deionized water containing only 1% sucrose. The esophageal carcinogen methylbenzylnitrosamine (MBN) was administered intragastrically in 10% ethanol twice per week for 5 wk at a dose of 2.5 mg/kg. MBN dosing was followed by a 12-wk period for tumor promotion. After this, heart, lungs, liver, spleen, kidneys, testes, tibia, muscle, brain and esophagus were excised. The esophagus was examined for MBN-induced lesions using dissecting and light microscopes and a portion was analyzed for Se. All other tissues were analyzed for Cu, Zn, Fe and Mn; some were also analyzed for Se and Mo. Most rats had precancerous lesions, and all rats had papillomas. There were no significant differences among the four treatment groups in the incidence and number per rat of precancerous lesions or gross papillomas. The SE group had significantly fewer carcinomas per rat than the other groups. The SE rats exhibited a number of significant differences in tissue trace element concentrations; in particular, they had higher Fe concentrations in heart, kidney and spleen than the other rats. The SE rats also had significantly greater urinary excretion of Mn and Fe, and excretion of the latter elements was significantly correlated with that of selenium.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1986

Hg- and Cu-induced hepatocellular changes in the mummichog, Fundulus heteroclitus.

To investigate mechanisms by which the mummichog (F. heteroclitus) successfully withstands heavy metal pollution, fish were treated with Hg2+ at up to 0.10 mg/L, Cu2+ at up to 1.0 mg/L, or combinations of Hg2+ and Cu2+. In earlier work, protein analysis of liver indicated that most of the cytosolic Cu is bound to the sulfhydryl-rich metallothionein, but that Hg is not associated with cytosolic proteins. Morphometric analysis indicates the Hg-treatment increases the lipid compartment of hepatocytes (ANOVA, F = 10.73, p less than 0.01). This lipid increase is correlated with the Hg content (analyzed by atomic absorption spectrophotometry) of individual liver samples (Spearman rank correlation, rs = 0.621, p less than 0.01). Cu treatment causes a reduction in the lipid compartment (F = 10.38, p less than 0.01), reduced cytoplasm in general (F = 18.55, p less than 0.001) and an increased lysosome count (F = 14.21, p less than 0.001). X-Ray microanalysis locates Cu in secondary lysosomes, but not in other organelles. Results of treatment with both Hg2+ and Cu2+ are similar to those of Hg2+ alone. Concentrations of Cu in liver varied too much to allow assessment of correlations with cytoplasmic changes. Usual mechanisms for handling toxic heavy metals include binding to metallothionein and sequestering in lysosomes. Our findings for Cu are in agreement with this. Fish, however, can methylate Hg. (We have found greater than 75% of killifish hepatic Hg to be methylated.) Increased cellular lipid may be a mechanism for sequestering the lipid-soluble methylmercury.

Animals↗
PubMed1984

Effect of a chelating drug on balance and tissue distribution of four essential metals.

Numerous drugs have structures that suggest that they and/or their metabolites are chelating agents, and therefore might affect trace metal metabolism. Ethambutol, used therapeutically in the treatment of tuberculosis, is an example. The objective of this study was to determine the effects of ethambutol on tissue concentrations and balance of 4 essential trace metals: copper, iron, manganese, and zinc. Eighteen male Sprague-Dawley rats (148 +/- 7 g) were housed individually in metabolic cages. Six rats received ethambutol (400 mg/kg/day) via the drinking water. There were 2 control groups of 6 rats each, an ad-lib and a pair-fed group. Iron concentrations in kidney, liver, heart, and spleen were significantly increased in both the pair-fed and ethambutol-dosed rats, an effect related to reduced food intake. However, the total iron content of these organs was comparable to that of the ad-lib controls, suggesting retention of iron by these organs with reduced food intake during growth. Trace element balance was not affected by ethambutol administration. Ethambutol produced significant decreases in heart copper, kidney zinc, plasma zinc, and liver copper and zinc not due to the associated reduced food intake. The latter results support the hypothesis that chelating drugs may alter trace metal metabolism.

Animals↗
PubMed1984

Effect of chronic ethanol ingestion on the metabolism of copper, iron, manganese, selenium, and zinc in an animal model of alcoholic cardiomyopathy.

Alcoholic cardiomyopathy (AC) is one of the diseases caused by alcohol abuse, and there has been considerable debate about the possibility that nutritional factors may be important in the etiology of AC. In addition, there is evidence that ethanol may affect the metabolism of trace elements. The purpose of this investigation was to determine if chronic ethanol administration produces changes in the metabolism of the essential metals copper, iron, manganese, zinc, and selenium using an animal model of AC. Eighteen male Sprague-Dawley rats were divided into three groups: an ad libitum control group (AL), a pair-fed control group (PF), and an ethanol-dosed group (ETOH). The latter group received gradually increasing concentrations (5-25%) of ethanol in the drinking water for 15 wk. Food intake was monitored and urine and feces collected for a 4-d period during the study to determine ethanol effects on trace-element balance. Growth of both the PF and ETOH animals was inhibited. Ethanol produced substantial increases in liver manganese and decreases in liver copper and zinc. Metal concentrations in heart and concentrations in other tissues studied (spleen, testes, brain, bone, kidney, and muscle) did not differ significantly among the groups, except for testes selenium and kidney zinc. Reduced food intake and ethanol ingestion were associated with a reduced percentage of ingested selenium excreted in the urine. Deficiencies of copper, iron, manganese, selenium, and zinc in myocardial tissue are not likely to be involved in the pathogenesis of AC in the rat.

Animals↗
PubMed1983

Vanadium, Na-K-ATPase, and potassium adaptation in the rat.

Vanadate is a potent inhibitor of Na-K-ATPase in vitro. It has been suggested that vanadium may function as a cellular regulator of Na-K-ATPase in vivo. To examine this speculation, we studied in rats the effect of high vanadate intake on 1) the tissue levels and distribution of vanadium, 2) basal activity of Na-K-ATPase in various tissues, and 3) the activity of Na-K-ATPase in various organs under conditions of massive chronic potassium loading known to stimulate Na-K-ATPase in the kidney and colon. Despite extremely high tissue levels of vanadium there was no demonstrable effect of the element on the basal activity of Na-K-ATPase. When subjected to chronic potassium loading, rats with high tissue vanadium concentrations underwent potassium adaptation that was associated with a rise in Na-K-ATPase activity in the renal cortex, renal medulla, and colonic mucosa. Further studies are needed to support or refute the thesis that vanadium might be an intracellular regulator of Na-K-ATPase in vivo.

Animals↗
PubMed1983

Vanadate effect on the Na,K-ATPase and the Na-K pump in in vitro-grown rat vascular smooth muscle cells.

The impact of vanadate on the Na,K-ATPase system in the vascular smooth muscle cell is poorly understood. The present study describes the kinetics of the effect of vanadate on Na,K-ATPase and the Na-K pump in in vitro grown rat VSMC's. Vanadate interaction with the Na,K-ATPase system in vascular smooth muscle cells was examined by observing its influence on ouabain-sensitive adenosine triphosphate hydrolysis in disrupted cells rendered permeable by osmotic shock, and the uptake of rubidium by intact cells. The I50 for vanadate inhibition of ouabain-sensitive hydrolysis of adenosine triphosphate occurred at vanadate concentrations of 10(-6) to 10(-7) M. This inhibition was potassium dependent. The maximal inhibitory effect of vanadate occurred at potassium concentrations of 10-20 mEq/liter. Sodium exerted a moderate antagonistic influence on vanadate inhibition of ouabain-sensitive adenosine triphosphate hydrolysis. Rubidium uptake by vascular smooth muscle cells was not altered within 120 minutes when 10(-5) M vanadate was added to the medium containing intact vascular smooth muscle cells. Yet, vanadium concentrations in the vascular smooth muscle cells within this incubation period reached levels 1.48-fold higher than the extracellular vanadate concentrations of 10(-5) M. These observations indicate that vanadate is a potent inhibitor of the VSMC Na,K-ATPase in disrupted vascular smooth muscle cells. However, in intact vascular smooth muscle cells vanadium gaining access into the vascular smooth muscle cell's interior does not inhibit the Na-K pump, probably because of its binding to intracellular proteins and/or conversion from the vanadate to the vanadyl ion.

Animals↗
PubMed1982

An apparent small cluster of choroidal melanoma cases.

Three choroidal melanomas were detected in a 2.5-year period in a small community of 3,592 persons. This small cluster represented an incidence about 20 times that expected (P = .0006). The community has an isolated water supply and very little industry. We determined the incidence of cancer in this and two adjacent communities and found no other unexpectedly high incidence. The three patients had no common exposures. Analyses of air and water from the involved community by mass spectroscopy, chromatography, and Ames (mutagenicity) tests were noncontributory. Nine of 60 mice given community water after weaning developed lens opacities eight to 16 months later; electron microscopy showed an abnormal monolayer of cells on the outer surface of the anterior lens capsule. The genesis of this monolayer was not clear. None of the 30 controls showed such lesions.

Adult↗