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Biomedical subjects

K L Stemmer

Publications and source records attributed to K L Stemmer.

18 recordsLinked to original sources
PubMed1990

Iron deficiency in growing male rats: a cause of development of cardiomyopathy.

Weanling male rats were fed a purified iron-adequate, a purified iron-deficient or a commercial diet for 12 weeks. At that time the rats were sacrificed, their hearts and livers were excised, and blood samples were taken. Heart and liver weights were recorded; organ tissue and serum samples were analyzed for Zn, Cu and Fe. Hemoglobin and hematocrit values were also obtained. The iron-deficient rats grew much more slowly than controls on the iron-adequate or commercial diets. The iron-deficient rats were severely anemic and had enlarged hearts (cardiomegaly). A histopathologic examination of the hearts of all animals showed that each heart of the iron-deficient rats had lesions characteristic of cardiomyopathy by dilatation, whereas none of the hearts of the iron-adequate group or the chow controls showed any lesions at all. The iron-deficient animals had only about 25% of the hepatic iron found in the iron-adequate animals but about 5 times the hepatic copper of the latter group or the chow controls. Heart iron of the iron-deficient group was 27% of the concentration found in hearts of the iron-adequate rats; heart copper was similar in all groups. Animals on the commercial stock diet accumulated significantly more iron in their hearts than did those on the purified iron-adequate diet but not in the livers. There was also a direct correlation of heart iron or heart zinc with log concentrations of dietary iron and consequently a direct correlation between heart iron and zinc concentrations.

Animals↗
PubMed1990

Interaction between aluminum and zinc or copper and its effects on the pituitary-testicular axis. II. Testicular enzyme and serum gonadotropin assay.

Sprague-Dawley male rats were divided into groups and maintained on a semipurified diet containing either 5 or 40 ppm of zinc or 2 or 8 ppm of copper. Half of the rats in each group received 1000 ppm aluminum in the diet. It was found that aluminum accumulated in the pituitary glands and testes when dietary copper levels were suboptimal. The ALP activity in testes was depressed by the added aluminum when the intake of zinc or copper was suboptimal. SDH, LDH, and LDH-X activities were inhibited and GRS and GGTP activities were elevated in rats fed either the suboptimal zinc or copper diet. However, the added aluminum in the diet reversed the changes to normal levels. The testosterone levels in plasma changed very little when the zinc or copper intake was suboptimal. An increase in plasma FSH was demonstrated in groups of both suboptimal zinc and copper intake. But the plasma LH was elevated only in the group receiving the suboptimal copper diet, and the added aluminum reversed plasma LH to control levels. A lower level of testosterone was demonstrated in the group given suboptimal copper with aluminum. It was concluded that dietary aluminum influenced the pituitary-testicular axis by interacting with certain essential trace metals, particularly zinc.

Aluminum↗
PubMed1990

Interaction of aluminum with zinc and copper and its effects on pituitary-testicular axis: a histological study.

To elucidate the interactions between aluminum and certain essential trace metals, an experiment was performed on rats fed diets with suboptimal or optimal levels of zinc or copper. Half of each group of animals were fed the same diet but with 1000 ppm aluminum added. Changes were noted after 120 days. Severe testicular damage was seen in rats fed either the low zinc or the low copper diet. The lesions included a wide range of spermatogenic cell degeneration and tubular atrophy. When aluminum was added to the diet, the testicular destruction of Zn-deficient rats was significantly reduced. This indicated that the presence of aluminum in the diet protected the testis against the damage caused by zinc deficiency. Pituitary glands were examined. Hypertrophy of basophiles was more pronounced in rats fed the suboptimal zinc or copper diet. When aluminum was added to their diet, the changes were reversed. The mechanisms by which aluminum protects male gonadal functions against Zn deficiency are discussed. This study is the first to demonstrate the preventive effect of aluminum against testicular damage caused by zinc deficiency.

Aluminum↗
PubMed1985

Copper deficiency effects on cardiovascular system and lipid metabolism in the rat; the role of dietary proteins and excessive zinc.

Weanling rats were fed a copper-deficient purified diet. The effects of varying the type of protein and supplements of copper and zinc on cardiovascular pathology and some biochemical parameters were investigated. It was found that cardiomyopathy developed in the copper-deficient groups. Milk powder caused significant exacerbation of this development relative to dietary casein or egg white. Angiopathy developed only when dietary zinc was 20 ppm. Dietary copper did not change this situation. Serum cholesterol was elevated when copper was low and casein or milk powder were the protein source. The data point to an interaction between type of protein and dietary copper or zinc in the pathogenesis of cardiovascular lesions.

Animals↗
PubMed1982

Activity of the enzymes dopamine-beta-hydroxylase and phenylethanolamine-N-methyltransferase in discrete brain regions of the copper-zinc deficient rat following aluminum ingestion.

We have investigated the possible interactions between the dietary intake of copper, zinc, or aluminum and the activities of the enzymes dopamine-beta-hydroxylase (DBH, EC.1.14.2.1) and phenylethanolamine-N-methyltransferase (PNMT, EC.2.1.1.28) in the male rat brain. Exposure to aluminum was for 120 days at 1000 ppm. The results showed that a diet suboptimal in copper or zinc decreased the activity of both enzymes in the three brain regions studied, including the frontal cortex, hippocampus, and cerebellum. The addition of aluminum to the suboptimal zinc diet restored the activity of both enzymes to within range of control values. The data are discussed with respect to an interaction between zinc and aluminum.

Aluminum↗
PubMed1981

Effect of ethanol on vinyl chloride carcinogenesis.

Four treatment groups (80 male Sprague-Dawley rats/group) were used in a 2 X 2 factorial design: inhalation of 600 ppm vinyl chloride (VC) 4 hr/day, 5 days/week for 1 year; VC and ingestion of 5% ethanol in water (v/v); filtered air and ethanol; filtered air. Ingestion of ethanol was begun 4 weeks prior to inhalation of VC and continued for life or termination of the study at two and one-half years from the first VC exposure. In this model system, ethanol potentiated the carcinogenic response to VC in the liver and produced an excess of neoplasms in animals receiving ethanol alone. Inhalation of VC induced angiosarcoma of the liver in 23% of the exposed animals; ethanol in addition to VC inhalation increased the incidence to 50%. Concomitant administration of VC and ethanol also produced an excess of hepatocellular carcinoma and lymphosarcoma. Ethanol with or without VC had a strong tumorigenic effect on the endocrine system. These results indicate that ethanol is a cocarcinogen in relation to the carcinogen VC.

Animals↗
PubMed1981

The influence of ingested aluminum upon norepinephrine and dopamine levels in the rat brain.

The clinical and neuropathological effects of elevated brain aluminum levels have only recently been described. The clinical symptoms, and localization of aluminum in the brain, suggest an altered catecholamine balance. We report the effects of elevated brain aluminum upon the endogenous steady-state levels of norepinephrine and dopamine in the frontal cortex, hippocampus and cerebellum. The neurotoxic effects of ingested aluminum are shown to be dependent upon the dietary intake of copper, zinc, iron, and magnesium. Norepinephrine levels in the cortex and cerebellum decreased in rats fed a low copper diet with aluminum added (0.1%, w/w). Suboptimal iron levels decreased norepinephrine in the cerebellum. The presence of aluminum in diets low in copper or zinc decreased dopamine levels in the cortex. The data are interpreted with respect to the clinical symptomatologies seen in demented, chronic renal dialysis patients with depressed serum copper and zinc levels.

Aluminum↗
PubMed1979

Cyanide toxicity from the thermal degradation of rigid polyurethane foam.

Thermal degradation products (tdp) from a model, rigid polyurethane foam were collected in such a manner as to eliminate carbon monoxide and other gases with low boiling points. The effects in rats resulting from intratracheal intubation (I.T.) of the tdp are discussed. Cyanide was found to be a major factor associated with severe toxic responses of the experimental rats.

Animals↗
PubMed1979

Some effects of oral ingestion of cadmium on zinc, copper, and iron metabolism.

Data are presented to show that ingestion of cadmium chloride by rats at low levels leads to alteration of zinc metabolism in the liver, even though the formation of metallothionein is not evident. A dose-response relationship between amount of cadmium ingested and degree of perturbation of zinc metabolism in liver was found. Oral cadmium was shown to cause emphysema and reduce pulmonary function in male rats; the effect was less severe or delayed in onset if dietary zinc concentration was high. Interference with copper and iron metabolism was shown to occur in rats given low levels of cadmium orally. Depression of copper and iron metabolism of the rat fetus was found to occur when dams received very low doses of cadmium during gestation, even though very little cadmium passed the placental barrier.

Animals↗
PubMed1975

Pulmonary response to polyurethane dust.

Weanling and 9 months or older rats were exposed to particles of an aged (PUF I) or freshly prepared (PUF II) rigid polyurethane foam by intratracheal intubation. The dose was 5 mg of particles. The response of the lung tissue was examined morphologically by serial sacrifices. Inflammation and macrophage activity were the initial responses. Fibrosis developed after 6 months. Nodular scars and perifocal emphysema were seen after 12 months. Four rats had a papillary adenoma in a major bronchus after 18 months exposure to PUF II.

Age Factors↗