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Biomedical subjects

G J Fosmire

Publications and source records attributed to G J Fosmire.

26 records · Page 2Linked to original sources
PubMed1976

Zinc deficiency in the weanling rat: effects on liver composition and polysomal profiles.

Some effects of zinc deficiency and inanition on post weanling development of the liver and on polysomal profiles were investigated. Failure to provide the weanling rat with adequate zinc resulted in anorexia, cyclical feeding, and growth retardation. Liver growth was also impaired, but was consonant with body size. Zinc deiciency resulted in a severe impairment of DNA accretion and a lowered concentration of RNA; protein alent to that for pair-fed controls, suggesting that the lowered protein concentration was largely due to inanition. In response to zinc deficiency, there was a smaller percentage of the total RNA on the gradient incorporated into the heaviest polysomal fraction. The amount of RNase activity did not appear to account for this altered polysomal distribution.

Animals↗
PubMed1975

Zinc deficiency during the latter third of pregnancy: effects on fetal rat brain, liver, and placenta.

The effects of zinc deficiency during the last third of gestation on the growth and development of the fetal rat at term were investigated. Zinc deficiency resulted in anorexia and weight loss of the pregnant dams. Fetuses from such dams displayed intrauterine growth retardation when compared with fetuses from pair-fed or ad libitum-fed controls given adequate zinc. Although the brains of the zinc-deficient fetuses were smaller than those of the controls, the brain was relatively spared while the liver was severely affected. The total cell number was reduced and there was an apparent increase in cell size in the brains of zinc-deficient fetuses in comparison with the brains of the controls. The growth failure of the zinc-deficient liver resulted in a smaller complement of total DNA, RNA, protein, and lipid, and there was less incorporation of [3H]thymidine into DNA in the liver. The placenta appeared to be only marginally affected by the zinc deficiency.

Animals↗
PubMed1975

Some effects of postnatal zinc deficiency on developing rat brain.

A deficiency of dietary zinc during the suckling period of the rat results in a depression in normal growth, which is, in part, due to the inanition experienced by the dam. The pups from such zinc-deficient dams have smaller forebrains at all of the time intervals investigated in comparison with pups from both zinc-adequate controls. The cell number of the forebrain of the zinc-deficient pup was also reduced in comparison with the zinc-adequate pups. RNA concentration did not appear to be affected, although the total RNA content was reduced because of the smaller brain size. The amount of protein per cell was reduced at 6 and 15 days in the zinc-deficient forebrain and polysomal profiles displayed abnormal distribution of material between monosomes and polysomes in the zinc-deficient brain. Zinc deficiency during the suckling period thus appears to disadvantage the animal in terms of body, brain growth, accretion of cells into the forebrain, and normal protein metabolism.

Age Factors↗
PubMed1975

Zinc deficiency and brain development in the rat.

Effects of prenatal and postnatal zinc deficiency on the composition of the brain and on subsequent adult behavior were studied. Deficiency throughout the latter third of pregnancy resulted in decreased body and brain size without affecting total brain DNA, RNA, or protein. Adult males that had been subjected to intrauterine zinc deficiency displayed impaired shock avoidance. Zinc deficiency from birth until 21 days of age resulted in impaired growth, decreased brain size, diminished brain DNA, RNA and protein. Cerebellar lipid concentration was also diminished. Such male animals displayed impaired maze acquisition as adults.

Animals↗
PubMedDate not supplied

Genetic influences on tissue deposition of aluminum in mice.

Aluminum is a known neurotoxin and has been suggested to play a role in the development of Senile Dementia of the Alzheimer's Type. The relationship between aluminum exposure and senile dementia cannot be a simple one, however, as not all exposure results in neurotoxic manifestations. To determine if there are genetic differences in susceptibility to moderate aluminum exposure, 16 mice of five inbred strains were divided into two groups. The control group was fed a purified diet containing all known requirements for mice; the experimental group was fed the same diet supplemented with 260 mg Al/kg diet for 28 d. Analysis of brains, livers, and tibias for aluminum concentrations revealed strain differences in response to dietary treatment. The most notable results occurred in the DBA/2 and C3H/2 strains, with brain aluminum levels higher in the experimental groups. In contrast, A/J, BALB/c, and C57BL/6 strains showed no differences in brain aluminum in response to dietary treatment. These findings suggest that there are genetic differences in the permeability of the blood brain barrier and lend support to the hypothesis that variability in aluminum toxicity may be, in part, genetically determined.

Aluminum↗