The effect of vitamin C supplementation on the development of organ pathology in experimental Trypanosoma brucei infection in rats was investigated. Infection caused significant (p<0.05) increases in serum alanine and aspartate aminotransferases as well as in blood urea nitrogen and serum creatinine. Infection also caused significant (p<0.05) hypoproteinemia and hypoalbuminemia as well as decreases in liver and kidney total homogenate proteins. Supplementation of infected rats with vitamin C prevented the disease-induced elevation of serum creatinine and alanine aminotransferase (ALAT) and also significantly ameliorated the decreases in total protein levels in serum, liver, and kidney, as well as the elevated serum aspartate aminotransferase (ASAT). The trypanosome infection caused depletion of the levels of reduced glutathione (GSH) in the blood, liver, and kidney, as well as reduced the plasma level of ascorbic acid. Vitamin supplementation prevented the depletion of these endogenous antioxidants. We concluded that vitamin C supplementation ameliorates oxidative stress, thereby sparing endogenous antioxidant reserves and protecting tissues and organs against T. brucei-induced damage.
Pyridoxine-deficient rats showed increased lipid peroxidation in the kidney when compared with control rats, and the lipid peroxidation was enhanced in the presence of inducers such as ascorbate and hydrogen peroxide. Pyridoxine-deficient kidney showed decreased levels of enzymic antioxidants such as glutathione peroxidase, superoxide dismutase, catalase, glutathione reductase, and glucose-6-phosphate dehydrogenase and non-enzymic antioxidants including ascorbate, glutathione and vitamin E. Treatment with the triterpenes—betulin and lupeol—restored the levels to normal, the latter being more effective in bringing about the changes.
We observed the effect of two soy isoflavones, i.e., daidzin, genistin, and soy extracts on femoral density and urinary bone resorption markers in ovariectomized stroke-prone spontaneously hypertensive rats (OVXSHRSP). Experiment 1: Twenty-five SHRSP, which were fed various soy isoflavones from the age of 5 weeks, were ovariectomized at the age of 19 weeks. Then 3 weeks later, the rats were sacrificed to examine their femurs. Experiment 2: Thirty-five SHRSP received an ovariectomy at the age of 19 weeks, and then various soy isoflavones were given for 2 weeks after the surgery. Twenty-four hour urine was collected before and for 2 weeks after ovariectomy. Femoral density in genistin- or soy extract-treated OVXSHRSP was significantly higher than in untreated OVXSHRSP. Urinary bone resorption markers, pyridinoline and deoxypyridinoline in OVXSHRSP fed genistin, daidzin, or soy extracts were significantly lower than those in untreated OVXSHRSP. These results indicate that soy isoflavones attenuate bone loss in OVXSHRSP.
Isolated rabbit hearts were subjected to hypothermic global ischemia for 1h and subsequent to normothermic Langendorff-reperfusion for 40min. Composition of the protein in the sarcoplasmic reticulum-enriched microsomal fraction was analyzed. Ischemia increased, whereas reperfusion decreased, the levels of a 65-kDa protein. The amino acid sequence in the N-terminal region of this 65-kDa protein was E-A-H-K-S-E-I-A-H-X-F-N-D-V-G-E-E, which resembled the antagonist protein (cytosolic Ca2+ uptake inhibitor antagonist protein) found in rabbit heart cytosol (Xu and Narayanan (1994) Mol. Cell. Biochem., 132, 7-14). Thus, ischemia may induce cytosolic albumin to associate with the microsomal fraction of cardiac membranes.
Protein affects many metabolic processes that are related to tissue growth. Effects of soy protein and casein diets on fecal enzyme activity and histochemistry of mucin of the colon were studied in the present experiments. Male mice were fed a soy protein or casein diet for one month (measurements by histochemistry) or for three weeks (measurements of fecal enzyme activity). Fecal β-glucosidase and β-glucuronidase activities were significantly higher in the mice fed the soy protein diet than in those fed the casein diet. There were significant differences in the histochemical morphology of the crypt of the colon stained with periodic acid Schiff (PAS), alcian blue (AB) at pH2.5, or high iron diamine/alcian blue (HID/AB) at pH2.5 between the mice fed the casein and those given the soy protein one. Granules strongly stained with PAS and AB were more numerous in the area from the middle to the upper part of the crypts in the mice fed the casein diet. However, in the mice fed the soy protein diet, the granules strongly stained with PAS and AB were widely distributed in the area from the lower to the upper part of the crypts. The difference in the histochemical morphology of the colonic crypts observed in our experiment might have been caused by a difference in the metabolism of microflora, by a difference in polyamine catabolism by the microflora, or by a different rate of colonic proliferation between the mice fed the soy protein and those fed the casein. These factors might be compounded to account for the difference in the histochemical morphology of the colonic crypt between the two dietary groups.
The amount of a 97-kDa protein in the sarcoplasmic reticulum-enriched microsomal fraction from rabbit heart changed in a manner dependent on the oxygenated condition after global hypothermic ischemia and subsequent normothermic reperfusion. Isolated hearts were immersed in physiologic saline for 0h (control group) or 1, 2 and 3h at 4°C (ischemia group) and were subjected to 40-min reperfusion at 37°C after 1h of hypothermic ischemia (reperfused group). The amount of the 97-kDa protein in the microsomal fraction apparently increased after ischemia, but decreased after reperfusion. The N-terminal amino acid of the protein was blocked and two internal sequences were determined, demonstrating the 97-kDa protein to be glycogen phosphorylase. A polyclonal antibody against rabbit skeletal muscular glycogen phosphor-ylase (GP) stained only the 97-kDa protein in the microsomal fraction in Western blot analysis. Microsomal fractions isolated from rabbit brain, liver, spleen, and white skeletal muscle were also examined by Western blot analysis using anti-GP. Liver and skeletal muscle contained a 97-kDa protein that reacted with anti-GP in control preparations. Ischemia induced a modest increase in the amount of the 97-kDa protein skeletal muscle microsomes, whereas no change in the amount of the protein occurred in liver microsomes. The results indicate that alteration in the energy metabolism from ischemia to the subsequent reperfusion is associated with the amount of GP.