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Biomedical subjects

K T Gottschall-Pass

Publications and source records attributed to K T Gottschall-Pass.

4 recordsLinked to original sources

Feeding rats diets enriched in lowbush blueberries for six weeks decreases ischemia-induced brain damage.

Oxidative stress is an important element in the etiology of ischemic stroke. Lowbush blueberries (Vaccinium angustifolium Aiton) have a high antioxidant capacity and thus we determined whether consumption of lowbush blueberries would protect neurons from stroke-induced damage. Rats were fed AIN-93G diets containing 0 or 14.3% blueberries (g fresh weight/100 g feed) for 6 weeks. Stroke was then simulated by ligation of the left common carotid artery (ischemia), followed by hypoxia. One week later, plasma and urine were collected, and neuronal damage in the hippocampus was determined histologically. In control rats, hypoxia-ischemia resulted in 40 +/- 2% loss of neurons in the hippocampus of the left cerebral hemisphere, as compared to the right hemisphere. Rats on blueberry-supplemented diets lost only 17 +/- 2% of neurons in the ischemic hippocampus. Neuroprotection was observed in the CA1 and CA2 regions, but not CA3 region, of the hippocampus. The blueberry diet had no detectable effects on the plasma or urine oxygen radical absorbance capacity (ORAC) or plasma lipids. We conclude that consumption of lowbush blueberries by rats confers protection to the brain against damage from ischemia, suggesting that inclusion of blueberries in the diet may improve ischemic stroke outcomes.

Animals↗

Zinc and the eye.

Zinc, a trace element that influences cell metabolism through a variety of mechanisms, appears to play an integral role in maintaining normal ocular function. This element is present in high concentrations in ocular tissue, particularly in retina and choroid. Zinc deficiency has been shown in a number of species to result in a variety of gross, ultrastructural and electrophysiologic ocular manifestations. The physiological functions for zinc have been studied predominantly in retina and retinal pigment epithelium where zinc is believed to interact with taurine and vitamin A. modify photoreceptor plasma membranes, regulate the light-rhodopsin reaction, modulate synaptic transmission and serve as an antioxidant. Suboptimal zinc status in North America may influence the development and progression of several chronic eye diseases. Zinc supplementation trials and epidemiological studies have produced conflicting results concerning the role of zinc in age-related macular degeneration. Additional well-controlled supplementation trials are indicated to clarify the role of zinc in this disease. Future investigations must also expand our understanding of the mechanisms by which zinc regulates ocular morphology and function.

Age Factors↗

Oscillatory potentials and light microscopic changes demonstrate an interaction between zinc and taurine in the developing rat retina.

Our objective was to investigate whether zinc interacts with taurine to influence the development of retinal structure and function. Virgin female Sprague-Dawley rats were bred overnight and assigned to one of four treatments in a 2 x 2 factorial design with two levels of zinc (50 micrograms/g through gestation and 50 micrograms/g after parturition; 15 micrograms/g through gestation and 7.5 micrograms/g after parturition) and two levels of taurine (2 or 0 mumol/g). The control diet contained 50 micrograms/g zinc and 2 mumol/g taurine. Guanidinoethyl sulfonate (10 g/L), a taurine transport inhibitor, was added to the drinking water of the rats receiving 0 mumol/g taurine. At postnatal d 23, male pups (n = 10) were weaned onto their respective diets. Pup eyes were examined by biomicroscope and indirect ophthalmoscope at 4 and 7 wk; retinal folds and choroidal atrophy were detected in the pups deficient in zinc and taurine. Analysis of plasma zinc and tibial zinc concentrations revealed a significant interaction in these tissues (P < 0.05). Dark-adapted oscillatory potentials (OP) were recorded at 7.5-8.5 wk. Two-way ANOVA showed a significant interaction between zinc and taurine for OP2 and OP3 amplitudes; marginal zinc deficiency decreased the amplitude of the OP only when rats were also deficient in taurine. A significant depressing effect of marginal zinc deficiency was noted for OP1 amplitude. Taurine deficiency significantly depressed the amplitude of OP1 and OP4. Histological examination of the retinas from rats deficient in both zinc and taurine revealed photoreceptor degeneration and confirmed retinal dysplasia. These data provide evidence for an interaction between zinc and taurine in retinal morphology and function.

Animals↗

Effect of taurine deficiency on tissue taurine concentrations and pregnancy outcome in the rat.

Taurine status and pregnancy outcome were assessed in rats fed low dietary taurine and varying doses of guanidinoethyl sulfonate (GES), a structural analogue of taurine. Female Sprague-Dawley rats (225-270 g) were mated overnight and assigned to one of four groups from day 0 to 20 of gestation. Taurine-deficient animals were fed a basal diet containing < 0.001 mumol taurine/g and 0.5 (n = 7), 1.0 (n = 8), or 2.0% (n = 7) GES in their drinking water, ad libitum. Control animals (n = 8) received similar treatment, with 2 mumol taurine/g added to the diet and no GES in their water. Taurine was analyzed by reverse-phase HPLC, using electrochemical detection after precolumn derivatization with ortho-phthalaldehyde. Treatment of rats with varying doses of GES produced a sharp decline in maternal liver and brain taurine to 15 and 55% of that of control levels, and in fetal liver and brain taurine to 75 and 50% of that of control levels, respectively (p = 0.0001; one-way ANOVA). The 2% group had a smaller mean (+/- SEM) litter weight than the control group (35.8 +/- 6.1 vs. 51.9 +/- 2.8 g; p = 0.042) as a result of a smaller litter size. The decrease in litter size was associated with confinement of implantation sites to either the left or right uterine horn in four of seven dams. Taurine deficiency did not result in intrauterine growth retardation or significant external, visceral, or skeletal malformations. Developmental defects were not found in any of the taurine-deficient groups, but reproductive abnormalities were present at the highest dose of the analogue.

Animals↗