The effect of fish oil treatment on the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase, and on the levels of lipid peroxides and glutathione of myocardial tissue was studied in isoproterenol-induced myocardial infarction. The biochemical lesion due to the activation of lipid peroxidation and decrease in antioxidant status could be significantly implicated in the experimental myocardial infarction induced by isoproterenol. The protective effect of fish oil was achieved by decreasing the peroxide concentration and the normalization of the levels of antioxidant defense enzymes.
The effect of pre-treatment with an alcoholic extract of Picrorhiza kurroa, a herbal drug, on D-galactosamine-induced hepatitis in rats was investigated with respect to the activities of serum marker enzymes, glycolytic enzymes, gluconeogenic enzymes, glucose-6-phosphate dehydrogenase, and membrane-bound ATPases and the levels of lipid peroxides and hepatic thiols. Prior oral treatment with P. kurroa extract significantly prevented the D-galactosamine-induced increases in the activities of serum marker enzymes, glycolytic enzymes, glycogen phosphorylase, and glucose-6-phosphate dehydrogenase and the decreases in the activities of key gluconeogenic enzymes and membrane-bound ATPases in the liver. The extract also exerted an antioxidant effect against D-galactosamine-induced hepatitis by blocking the induction of lipid peroxidation and by preventing the depletion of hepatic thiols. The present findings confirm that P. kurroa is hepatoprotective in experimentally induced hepatitis in rats.
To evaluate the effects of voluntary resistance exercise and aerobic exercise on iron status in rats fed an iron-deficient diet (5mg Fe/kg, ID) or rats fed a control diet (35mg Fe/kg, CN), we trained female Wistar rats for 3 weeks to climb a wire-mesh tower (∅20cm×200cm, CLIMB) and to swim in a plastic pool (∅50cm×50cm, SWIM). These animals were compared with sedentary (SED) rats. After the experimental period, the blood hemoglobin concentration, hematocrit, plasma iron, and transferrin saturation were significantly lower (p<0.05) in the ID rats than in the CN rats; as was the content in the liver, spleen, heart, kidney, skeletal muscles, and carcass (p<0.05). The activity of δ-aminolevulinic acid dehydratase, the marker enzyme for heme biosynthesis, in bone marrow was significantly higher (p<0.05) in the CLIMB group than in the SWIM group. These results suggest that resistance exercise increases heme biosynthesis more than aerobic exercise but that neither exercise improved severe iron deficiencies.
It has been established that there are two isoforms of mammalian branched-chain aminotransferases, cytosolic (BCATc) and mitochondrial (BCATm). Since the BCATc was reported to be a direct target for c-Myc regulation, we investigated expression of mRNAs for c-myc, BCATc, and BCATm in human gastric cancer cells and tissues. MKN45 and KATOIII were used as human gastric cancer cell lines. Human gastric mucosal tissues with cancer were obtained from 9 patients and those with non-ulcer dyspepsia (NUD) were from 8 patients by endoscopic biopsy. Expression of mRNA was measured by the method of polymerise-chain reaction coupled with reverse transcription. Expression of c-myc mRNA was detected in both cell lines but was greater in MKN45. Expression of BCATc mRNA was detected in KATOIII, but not in MKN45, whereas expression of BCATm mRNA was detected only in MKN45. In the analyses of human gastric tissues, it was found that c-myc mRNA was expressed in all of the tissues examined, but overexpression of the mRNA was detected in the 5 tissues with cancer. On the other hand, expression of BCATc mRNA was detected in 4 tissues with gastric cancer, in which only one tissue had the overexpression of c-myc mRNA. Expression of BCATc mRNA was not detected in all tissues with NUD. BCATm mRNA expression was detected in all tissues with cancer or NUD. These results suggest that there is no correlation between expression of mRNAs for c-myc and BCATc in these tissues and that expression of BCATc in gastric cancer cells and tissues is regulated in a manner independent of c-myc expression.
Menkes' disease is an inherited disorder of copper homeostasis that arises from a deficiency in copper-transporting P-type ATPase, the mouse gene for which is designated Atp7a. The macular and the viable-brindled mouse are among Menkes' disease models and have been shown to have respective single missense mutations in their genes. In this study we tested whether these mutations are a cause of the disease. Yeast strain Δccc2, lacking CCC2, the yeast homologue of Atp7a, was used to examine whether this mutant yeast can be rescued by expression of acular or viable-brindled Atp7a protein when cultured in copper- and iron-deficient medium. Expression of both mutant Atp7a proteins was found to enable the growth of Δccc2 yeast, but the growth rates were less than one-fifth of the rate observed for Δccc2 yeast expressing wild-type Atp7a protein. Thus it is clear that the missense mutations of both animal models for Menkes' disease are responsible for the impaired function of copper transport.