Showing papers on "Isotopes of chromium published in 1984"
TL;DR: This in vitro model indicates that paraquat-induced type II cell injury can be quantified, confirmed by morphologic ultrastructural changes, significantly reduced by antioxidants, and potentiated by hyperoxia.
Abstract: Paraquat, a widely used herbicide, causes severe, often fatal lung damage. In vivo studies suggest the alveolar epithelial cells (types I and II) are specific targets of paraquat toxicity. This study used 51Cr-labeled type II cells to demonstrate that paraquat (10-5 M) resulted in type II cell injury in vitro, independent of interacting immune effector agents. With 51Cr release expressed as the cytotoxic index (Cl), type II cell injury was found to accelerate with increasing paraquat concentrations (10(-5) M, 10(-4) M, and 10(-3) M, resulting in a Cl of 12.5 +/- 2.2, 22.8 +/- 1.8, and 35.1 +/- 1.9, respectively). Paraquat-induced cytotoxicity (10(-4) M, with a Cl of 22.8 +/- 1.8) was effectively reduced by catalase 1,100 U/ml (Cl 8.0 +/- 3.2, p less than 0.001), superoxide dismutase, 300 U/ml (Cl 17.4 +/- 1.7, p less than 0.05), alpha tocopherol, 10 micrograms/ml (Cl 17.8 +/- 1.6, p less than 0.05). Paraquat toxicity (10(-3) M) was potentiated in the presence of 95% O2 with an increase in Cl from 31.1 +/- 1.7 to 36.4 +/- 2.3 (p less than 0.05). Paraquat-induced type II cell injury was noted as early as 4 h incubation by electron microscopic evidence of swelling of mitochondrial cristae and dispersion of nuclear chromatin. Thus, this in vitro model indicates that paraquat-induced type II cell injury can be quantified, confirmed by morphologic ultrastructural changes, significantly reduced by antioxidants, and potentiated by hyperoxia.
23 citations
TL;DR: The results indicate that the placentofetal unit is capable of extracting large amounts of Cr from the mother, and support the suggestion that maternal Cr is depleted during pregnancy, and suggest that body tissues may defend their Cr stores against Cr depletion by adaptive cellular Cr transport mechanisms.
Abstract: Since trivalent chromium (Cr+3) transport into certain tissues is rapid, the placental transport of injected high specific activity 51Cr+3 was studied in pregnant rats at days 17-20 of gestation. Three days after the intravenous injection of 51Cr+3, body retention of 51Cr was similar in pregnant and nonpregnant rats, but in the pregnant rats placentofetal uptake of 51Cr accounted for 25-30% of the 51Cr retention. The mean 51Cr content per placentofetal unit was 0.89 +/− 0.03% injected dose. Serum and tissue 51Cr contents per milliliter or gram in the pregnant rats were decreased by 50-80% except in uterus, which was unchanged. Tissue/serum 51Cr ratios were increased by 70-300% in the pregnant rats compared to the nonpregnant controls. These results indicate that the placentofetal unit is capable of extracting large amounts of Cr from the mother, and support the suggestion that maternal Cr is depleted during pregnancy. The data also suggest that body tissues may defend their Cr stores against Cr depletion ...
18 citations
TL;DR: It is suggested that cellular energy stores are being depleted by the influx of chromium, which is a response to an intracellular deficit or uncoupling of metabolic pathways.
Abstract: Following thermal injury neutrophil function is severely impaired and thought to be hypometabolic; however, the host is considered to be hypermetabolic. To further investigate the metabolism and the function of neutrophils following thermal injury, neutrophil migration and chromium uptake were studied using radio-labelled neutrophils. Random and directed migration were found to be significantly reduced compared to control values. Neutrophil lysozyme content was also reduced in these burn cells while serum lysozyme from the same patients was significantly elevated over control values. These data suggest lysozyme is released by the neutrophil into the circulatory system. The influx of chromium in cells from burned patients was much greater than the influx in normal cells used in studies for chemotaxis. Influx of chromium over time and over varying concentrations of chromium was linear in cells from burned patients and normals. Cells from burned patients, however, took up more chromium than normals. Influx velocity of chromium was also determined and found to be greater in burn cells than normal cells. Since it has been shown that chromium influx is an energy-dependent reaction it is suggested that cellular energy stores are being depleted by the influx of chromium. Whether this is a response to anmore » intracellular deficit or uncoupling of metabolic pathways is not known at this time.« less
4 citations