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761.
Pi depletion of proximal tubule cells isolated from mouse kidney results in a decrease in the cell content of fructose-2,6-bisphosphate and an increase in the rate of gluconeogenesis from pyruvate, malate and succinate. Gluconeogenesis from glycerol is unaffected by Pi depletion. Introduction of fructose-2,6-bisphosphate into the cytosol of ATP-permeabilized cells is accompanied by a fall in gluconeogenesis. The presence of external Ca2+ stimulates gluconeogenesis. When cytosolic Ca2+ is raised to 1.8 microM by permeabilization, the resealed cells still require 2.5 mM Ca2+ in the bathing medium in order to perform gluconeogenesis at the maximum rate. Cells permeabilized in the presence of cAMP show a decreased rate of glucose production. Phorbol ester stimulates gluconeogenesis provided that the phorbol treatment is performed in the absence of Ca2+ ions. It is suggested that Pi depletion may stimulate pyruvate carboxylase activity and facilitate the entry of certain gluconeogenic substrates into mitochondria. It is also proposed that important aspects of the control of renal gluconeogenesis by parathyroid hormone are mediated by protein kinase C. 相似文献
762.
Cultured cardiac myocytes were depleted of ATP by incubation with oligomycin (1 mg/ml). Then the ability of the cells to oxidize various substrates and to restore ATP levels was studied. Following ATP depletion, the cells were found to be able to oxidize glucose given alone, but not palmitate. However, with both substrates, palmitate was oxidized in the presence of glucose and ATP recovery was enhanced. Pyruvate had a minor effect on palmitate oxidation, while acetate given alone was oxidized, but did not enhance cellular ATP content. These results show that glucose is essential for restoration of mitochondrial function and the coupling between oxidation and ATP synthesis. 相似文献
763.
Cadmium-induced excretion of urinary lipid metabolites,DNA damage,glutathione depletion,and hepatic lipid peroxidation in sprague-dawley rats 总被引:7,自引:0,他引:7
Recent studies have described lipid peroxidation to be an early and sensitive consequence of cadmium exposure, and free radical
scavengers and antioxidants have been reported to attenuate cadmium-induced toxicity. These observations suggest that cadmium
produces reactive oxygen species that may mediate many of the untoward effects of cadmium. Therefore, the effects of cadmium
(II) chloride on reactive oxygen species production were examined following a single oral exposure (0.50 LD50) by assessing hepatic mitochondrial and microsomal lipid peroxidation, glutathione content in the liver, excretion of urinary
lipid metabolites, and the incidence of hepatic nuclear DNA damage. Increases in lipid peroxidation of 4.0- and 4.2-fold occurred
in hepatic mitochondria and microsomes, respectively, 48 h after the oral administration of 44 mg cadmium (II) chloride/kg,
while a 65% decrease in glutathione content was observed in the liver. The urinary excretion of malondialdehyde (MDA), formaldehyde
(FA), acetaldehyde (ACT), and acetone (ACON) were determined at 0–96 h after Cd administration. Between 48 and 72 h posttreatment
maximal excretion of the four urinary lipid metabolites was observed with increases of 2.2- to 3.6-fold in cadmium (II) chloride-treated
rats. Increases in DNA single-strand breaks of 1.7-fold were observed 48 h after administration of cadmium. These results
support the hypothesis that cadmium induces production of reactive oxygen species, which may contribute to the tissue-damaging
effects of this metal ion. 相似文献