摘要:

Young adult female mice were injected with lead acetate (d 0). Following injection, determinations were made of the percentages of radioactive iron (59Fe) uptake into the hemoglobin of erythrocytes produced by spleen. Control59Fe uptake percentage vacillated between 4.2 and 5.5 within the 7‐d period of observation. On d 4 following lead treatment, splenic percentages were dramatically reduced below those of the saline‐injected controls; by d 6 the splenic59Fe uptake of lead‐treated mice was comparable to that of controls. For rodents injected with cadmium chloride on d 0, the59Fe uptake values showed a statistically significant elevation by d 2, which was extended beyond that of the controls’ d 4 value. For those animals receiving both lead and cadmium (d 0), the uptake percentages paralleled those of the controls throughout the 7‐d period of observation. These data suggest that the inhibitory effect of lead on erythropoiesis of the spleen is blocked by a concurrent cadmium treatment. Results are interpreted in regard to a possible vulnerable target and competition for the target by lead and cadmium.

ISSN:0098-4108    

DOI:10.1080/15287399209531588

出版商:Taylor & Francis Group    

年代:1992

数据来源: Taylor

摘要:

The liver is the major organ responsible for ethanol oxidation, and alcohol dehydro‐genase (ADH) is the main enzyme involved. There is limited evidence suggesting the involvement of the lung in ethanol metabolism. To determine the degree to which pulmonary ADH plays a role in ethanol metabolism, ADH activity was measured spectrophotometrically using hepatic and pulmonary cytosolic fractions prepared by differential centrifugation and Sephadex G‐50 column chromatography. Apparent Kmvalues for hepatic and pulmonary ADHs were determined. Inhibition constants were calculated using 4‐methylpyrazole. The ADHs were characterized by examining the influence of pH on enzyme activity. Pulmonary ADH activity was much lower at near neutral pH than at pH 9.0 or 10, whereas hepatic ADH activity was also pH dependent but was significantly higher. Pulmonary ADH is less sensitive to inhibition by 4‐methylpyrazole than is hepatic ADH, as evidenced by a 1000‐fold higher Ki. Pulmonary ADH would be expected to make only a minor contribution to ethanol metabolism in vivo.

ISSN:0098-4108    

DOI:10.1080/15287399209531589

出版商:Taylor & Francis Group    

年代:1992

数据来源: Taylor

摘要:

The metabolism of butachlor was studied in rat liver and kidney homogenates. In vitro incubation of butachlor with liver fractions (S9, microsome, and cytosolic fractions) formed a considerable amount of butachlor glutathione conjugate (BGSC), while the conjugating activity was not efficient for the kidney S9 fraction. There is a sex difference in the distribution of glutathione S‐transferase in the liver. It seems that more enzyme activity is detected in the female liver microsome, while this is not the case in its cytosolic fraction. Further biotransformation of BGSC to mercapturate was not observed in the liver S9 fraction. This metabolite was further transformed to butachlor acetyl cysteine conjugate (BACC) in the presence of acetyl CoA, but to buta‐ chlor cysteine conjugate (BCC) in the absence of acetyl CoA. These findings demonstrated that butachlor is initially conjugated with CSH to form BGSC by the enzyme glutathione S‐transferase in the liver. This metabolite is apparently transported to the kidneys, where it is transformed to the mercapturate.

ISSN:0098-4108    

DOI:10.1080/15287399209531590

出版商:Taylor & Francis Group    

年代:1992

数据来源: Taylor

摘要:

The half‐life of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD), the contaminant of Agent Orange, has been recently estimated in 36 members of Operation Ranch Hand, the Air Force unit responsible for the aerial spraying of Agent Orange in Vietnam, as 7.1 yr with a 90% confidence interval of 5.8–9.6 yr. We investigated the variability of TCDD half‐life with percent body fat in these 36 Ranch Hand veterans who have two TCDD assay results from serum drawn in 1982 and 1987. Using a repeated measures linear model, we found a marginally significant change in half‐life with percentage of body fat (p ‐ .09) and no statistically significant change in half‐life with relative changes in percentage of body fat from 1982 to 1987 (p ‐ .60).

ISSN:0098-4108    

DOI:10.1080/15287399209531591

出版商:Taylor & Francis Group    

年代:1992

数据来源: Taylor

摘要:

It has been suggested that radicals on the surface of dust particles are key chemical factors in the pathophysiology that results from the occupational inhalation of coal and silica dust. In addition, oxygenated derivatives of arachidonic acid (eicosanoids) have been implicated as important biochemical mediators of mineral dust‐induced lung disease through their role in bronchial and vascular smooth muscle reactivity, inflammation, and fibrosis. Therefore, we assessed eicosanoid production by the rat alveolar macrophage (AM) exposed in vitro to mineral dusts with varying surface chemical characteristics in order to determine if radicals associated with the mineral dust could influence the production of proinflammatory mediators in the lung environment. Primary cultures of rat AM were exposed to freshly fractured or “stale” bituminous coal dust, as well as untreated silica or silica calcined to 500 and 1100°C. Prostaglandin E2(PGE2), thromboxane A2(TXA2), and leukotriene B4(LTB4) levels in incubation medium were determined by specific radioimmunoassay. When AM were exposed to freshly fractured coal dust, PGE2production was markedly increased. In contrast, exposure of AM to “stale” dust significantly reduced PGE2production. Exposure of AM to freshly fractured coal dust resulted in a significant increase in production by AM, while exposure to stale coal dust did not influence AM TXA2production. Neither “fresh” nor “stale” coal dust had any effect on LTB4production. In vitro exposure of AM to untreated silica resulted in a significant increase in TXA2PCE^ TXA2, and LTB4production compared with control. However, exposure of AM to silica calcined to 1100°C resulted in eicosanoid levels that were not significantly different from control. These effects were still apparent 8 wk after calcination of the silica particles. Silica was a more potent activator of AM eicosanoid production than was coal, and amorphous fumed silica was a more potent activator of AM eicosanoid production than was crystalline silica. These findings suggest that radicals associated with respirable coal and silica particles may play a key role in the ability of mineral dust to activate AM eicosanoid production and therefore may be important in the pathophysiological consequences of occupational mineral dust inhalation.

ISSN:0098-4108    

DOI:10.1080/15287399209531592

出版商:Taylor & Francis Group    

年代:1992

数据来源: Taylor

摘要:

The purpose of this study was to determine if Zn pretreatment could protect rat primary hepatocyte cultures from the cytotoxicity of five metals that have little or no affinity for metallothionein (MT). Hepatocytes were grown in monolayer cultures for 22 h and subsequently treated with ZnCI2(100 μM) for 24 h; which increased the MT concentration 15‐fold. Following Zn pretreatment, hepatocytes were exposed to various concentrations of Mn, V, Cr, Se, or Fe for an additional 24 h. Cytotoxicity was assessed by enzyme leakage and loss of intracellular K+. The toxicity of all five metals was significantly reduced in the Zn‐pretreated cells. Zn pretreatment had no appreciable effect on the hepatocellular uptake (1–24 h) of Mn or Se. Zn pretreatment also did not increase the distribution of Mn or Se to the cytosol and neither metal was bound to MT, suggesting the protection was not due to their binding to MT. However, Zn pretreatment significantly decreased Mn‐, Cr‐, and V‐induced cellular glutathione depletion. In summary, Zn pretreatment of rat primary hepatocyte cultures protects against Cr‐, Mn‐, Fe‐, Se‐, or V‐induced hepatotoxicity. This protection does not appear to be related to MT induction but may be due to Zn‐induced thiol or membrane stabilization and/or other biological changes produced by Zn.

ISSN:0098-4108    

DOI:10.1080/15287399209531593

出版商:Taylor & Francis Group    

年代:1992

数据来源: Taylor

摘要:

Cigarette smoke has been demonstrated to suppress the biosynthesis of connective tissue in the lung. To further characterize this suppressant effect, we studied the ability of cigarette smoke to prevent or ameliorate cadmium‐induced alterations in rat lungs in vivo. The effects of ß‐aminopropionitrile (ßAPN), an agent that inhibits the cross‐linking of elastin, also were studied. Eighty‐eight young female Long‐Evans rats were randomly divided into seven groups as follows: control, cigarette smoke, sham smoke, ßAPN, cadmium, cadmium + cigarette smoke, and cadmium + ßAPN. Each animal in the cigarette smoke group was exposed to mainstream smoke generated from University of Kentucky 2R1 reference cigarettes (10 puffs daily for 12 wk). Sham‐treated animals received room air in place of cigarette smoke. ßAPN (0.5 g/kg) was injected intraperitoneally twice weekly. In cadmium‐treated groups, each rat received intermittently three intratracheal instillations of cadmium chloride (0.15 nmol/kg) over a 5‐d period. For the cadmium + cigarette smoke group, smoke exposure began 3 d after the first cadmium instillation and was continued for 12 wk. The ßAPN administration began 5 d before cadmium instillation and also was continued for 12 wk. After these treatments, pulmonary function and lung morphometry were examined. Neither cigarette smoke, sham smoke, nor ßAPN produced significant changes in lung function or morphometry. Cadmium caused significant decreases in total lung capacity, dynamic and static compliance, and carbon monoxide diffusing capacity, as well as significant increases in lung weight and alveolar wall thickness. In addition, the quasi‐static deflation pressure‐volume curve showed a rightward shift whereas the mean linear intercept of the alveoli did not change significantly. Efforts to prevent or ameliorate the changes through exposure to cigarette smoke or administration of ßAPN were unsuccessful. It is concluded that interventions designed to inhibit the biosynthesis of lung connective tissue do not perforce inhibit the development of cadmium‐induced pulmonary changes in the rat.

ISSN:0098-4108    

DOI:10.1080/15287399209531594

出版商:Taylor & Francis Group    

年代:1992

数据来源: Taylor

摘要:

TRACE ELEMENTS IN HEALTH AND DISEASE: Proceedings of the International Symposium on Trace Elements in Health and Disease, Espoo, Finland, June 5–8, 1990. Edited by Antero Aitio, Antti Aro, Jorma Järvisalo, and Harri Vainio. The Royal Society of Chemistry, United Kingdom, 1991. 236 pp., £45.00

ISSN:0098-4108    

DOI:10.1080/15287399209531595

出版商:Taylor & Francis Group    

年代:1992

数据来源: Taylor

ISSN:0098-4108    

DOI:10.1080/15287399209531587

出版商:Taylor & Francis Group    

年代:1992

数据来源: Taylor