摘要:

In May 1981, a massive intoxication of people who had ingested adulterated cooking oil took place in Madrid and nearby provinces. Although the patients presented, in the first phase of the disease, with acute respiratory illness, later on thromboembolic com‐plications, severe neuromuscular involvement, and scleroderma‐like cutaneous lesions appeared. Kidneys were apparently spared; however, 4 out of 842 admitted patients developed glomerulonephritis; kidney biopsies revealed glomerular, vascular, tubular, and interstitial changes. Cases 1 and 3 had diffuse proliferative endocapillary glomerulonephritis; case 2 had diffuse membranoproliferative glomerulonephritis; and case 4 had diffuse extracapillary glomerulonephritis. Three cases had vasuclar lesions characterized by degenerative and proliferative endothelial changes, intimai foamy macrophages, and partial or complete obliteration of the vascular lumen by concentric myxoid fibrosis. There were signs of necrosis of tubular epithelium along with edema and lymphocytic and eosinophilic interstitial infiltration. Two out of 22 autopsies had segmentary glomerulonephritis, and 17 out of 22 autopsies showed renal vascular lesions.

ISSN:0098-4108    

DOI:10.1080/15287398409530477

出版商:Taylor & Francis Group    

年代:1984

数据来源: Taylor

摘要:

Human adipose tissue samples obtained during autopsies in a Canadian Great Lakes community, Kingston, Ontario, and a second community, Ottawa, Ontario, were analyzed for organochlorine pesticides, polychlorobiphenyls, chlorobenzenes, and chlorophenols. Significantly different levels of Dichlorodiphenyl‐dichloroethane, mirex, hexachlorobenzene, and 2,3,4,6‐tetrachlorophenol were found in Kingston adipose tissues compared to Ottawa tissues. Residue levels of oxychlordane, mirex, and poly‐chlorinated biphenyls were significantly different in Kingston males versus Kingston females. The means and ranges of residue levels were contrasted with those reported in previous Canadian surveys.

ISSN:0098-4108    

DOI:10.1080/15287398409530478

出版商:Taylor & Francis Group    

年代:1984

数据来源: Taylor

摘要:

The effects on the immune system of rats that had been exposed to a 2‐mg/m3 dose of either respirable coal dust, diesel exhaust fumes and particulates, or the combination of these were studied. Animals that were housed similarly but exposed only to filtered air served as controls. After 12 and 24 mo of exposure, the rats were tested for immunocompetency by enumerating antibody‐producing cells in the spleen 4 d after immunization with sheep erythrocytes and by monitoring the proliferative response of splenic T‐lymphocytes to the mitogens concanavalin A and phytohemagglutinin. The results of this study indicate that no major alterations occurred in the immunologic functions measured as a result of exposure to either coal dust, diesel exhaust fumes and particulates, or their combination.

ISSN:0098-4108    

DOI:10.1080/15287398409530479

出版商:Taylor & Francis Group    

年代:1984

数据来源: Taylor

摘要:

Benzo[a]pyrene, a lipophilic promutagen, reached maximal concentrations in the thoracic duct lymphatic circulation within 2 h after gastric instillation. Benzo[a]pyrene in lymph obtained by thoracic duct cannulation decreased to approximately control levels within 4 h after treatment. When lymph was not allowed to enter the blood vascular circulation, serum levels of benzofajpyrene increased very slowly, suggesting minimal mesenteric blood vascular absorption of the lipophilic hydrocarbon. Benzo[a]pyrene partitions into lymph Iipoproteins as a function of the lipoprotein concentration. Data suggest that low‐density lipoproteins may take up benzofajpyrene more efficiently than do very low‐density or high‐density lipoproteins, and that lymph components other than lipoproteins do not take up and transport benzofajpyrene. We propose that lipophilic xenobiotic compounds interact with cells of the immune system via lymphatic lipoprotein transport of potentially mutagenic, carcinogenic, or immuno‐suppressive agents.

ISSN:0098-4108    

DOI:10.1080/15287398409530480

出版商:Taylor & Francis Group    

年代:1984

数据来源: Taylor

摘要:

Benomyl, a systemic fungicide, was administered to male Sprague‐Dawley rats during the prepuberal, pubertal, or postpubertal stage of reproductive development. Animals received 5 or 10 daily treatments of 0, 125, 200, 250, 500, or 1000 mg benomyl/kg‐d by gavage. Observations were made at selected intervals after exposure and included hematological parameters, body weight, tissue weights, total epididymal sperm counts, vas deferens sperm concentration, serum follicle‐stimulating hormone (sFSH) levels, and testicular histology. Data presented here suggest that there is an age‐related difference in sensitivity to benomyl. Animals that received benomyl treatments during prepuberty showed no significant treatment effects in tissue weights, total epididymal sperm counts, vas deferens sperm concentration, or sFSH. Animals that received at least 250 mg/kg‐d during puberty or postpuberty showed one or more of the following effects: decreased testicular or epididymal weights, decreased epididymal sperm count, decreased vas deferens sperm concentrations, and/or testicular lesions. Histological examination of testicular tissue indicated a higher incidence of diffuse hypospermato‐cytogenesis in pubertal (20% of the treated animals) and postpubertal (40% of the treated animals) animals that were exposed to benomyl. These values were compared with those of the treated prepubertal animals, which had a 10% incidence of diffuse hypospermatocytogenesis, and with all of the control animals, which had no occurrences of this testicular lesion.

ISSN:0098-4108    

DOI:10.1080/15287398409530481

出版商:Taylor & Francis Group    

年代:1984

数据来源: Taylor

摘要:

Paraquat inhibits thein vitrohepatic microsomal metabolism of both ethylmorphine and aniline. Inclusion of ascorbate with paraquat in the incubations did not alter the paraquat effect on ethylmorphine N‐demethylase activity but potentiated the inhibition of aniline p‐hydroxylase activity. Ascorbate alone was without effect on the metabolism of either substrate. Paraquat stimulated the hepatic microsomal oxidation of nicotinamide adenine dinucleotide phosphate (NADPH) equally in the absence of mixed‐function oxidase (MFO) substrates or in the presence of ethylmorphine; in the presence of aniline the rate of NADPH oxidation was significantly greater. Also, in the presence of aniline, ascorbate potentiated the paraquat‐induced NADPH oxidation, while it was ineffective with paraquat on NADPH oxidation in the presence of ethylmorphine or in the absence of substrates for the microsomal MFO system. The potentiated inhibition of aniline metabolism, concomitant with the potentiated stimulation of NADPH oxidation, was consistent whether liver microsomal fractions were prepared from control rats or from animals induced with phenobarbital. Investigation of possible influences on NADPH cytochrome c reductase activity was precluded by the rapid nonenzymatic reduction of cytochrome c by ascorbate. The paraquat‐ascorbate redox couple would not reduce cytochrome P‐450. These data suggest that a paraquat interaction with the active microsomal MFO enzyme system plays a role in the depletion of cellular NADPH stores that occurs after paraquat administrationin vivo. This mechanism may play a significant role in the development of paraquat toxicity and in the potentiated toxicity observed with ascorbate and paraquat.

ISSN:0098-4108    

DOI:10.1080/15287398409530482

出版商:Taylor & Francis Group    

年代:1984

数据来源: Taylor

摘要:

Groups of 93 male and 93 female Sprague‐Dawley rats were fed diets containing 1, 5, 25, and 250 ppm fenvalerate for up to 2 yr. The control group consisted of 183 males and 183 females. Approximately 10 treatment and 20 control rats/sex‐group were killed at Intervals of 3, 6, 12, and 18 mo. When body weights, food consumption, hematology, clinical chemistry and organ weights did not reveal a treatment effect, two additional groups of 50 males and 50 female rats were placed on 0 or 1000 ppm fenvalerate diets and maintained for 2 yr. Body weight was decreased and organ/body weight ratios were increased in brain, liver, spleen, kidneys (females), heart (females), and testes (males) in the 1000 ppm group. Mammary and pituitary tumors were commonly observed, along with a variety of other tumors occurring randomly among all control and treatment groups. No statistically significant differences in the number and type of neoplasms were observed except for mammary tumors in females in the main study. These effects were judged not to be toxicologically significant, since mammary tumor incidences did not exceed expected incidences in aged female Sprague‐Dawley rats, time to tumor appearance was unchanged, and no shift in percent benign versus malignant tumors occurred. Sarcomas identified in the subcutis and dermis in 5/51 1000‐ppm‐treated males were also identified in 2% (1/50), 2% (2/102), and 0–6% of concurrent, original, and historical controls, respectively. Microscopic examination did not reveal any treatment‐related lesions. The no‐observable‐effect level was determined to be 250 ppm.

ISSN:0098-4108    

DOI:10.1080/15287398409530483

出版商:Taylor & Francis Group    

年代:1984

数据来源: Taylor

摘要:

Experiments were conducted to test the hypothesis that the hepatocarcinogenicity of di(2‐ethylhexyl) phthalate (DEHP) is due to its ability to produce DNA damage, either directly or as a result of the proliferation of peroxisomes and accompanying increased production of H2O2 and other DNA—damaging oxygen radicals induced by sustained exposure to the plasticizer. DNA repair, as assessed by the autoradiographic measurement of unscheduled DNA synthesis (UDS), was not observed in primary rat hepatocytes exposedin vitroto 10–5‐10–2 M DEHP orin vivoby a single gavage dose of 5 g DEHP/kg body weight administered 2, 15, or 24 h prior to the isolation of hepatocytes. Thus, DEHP does not appear to directly produce repairable DNA damage in rat hepatocytes.

ISSN:0098-4108    

DOI:10.1080/15287398409530484

出版商:Taylor & Francis Group    

年代:1984

数据来源: Taylor

摘要:

Early alterations in normal semiconservative and repair DNA synthesis were determined in gastrointestinal tissues of Ha/CR mice following administration of the colon carcinogen 1,2‐dimethylhydrazine (DMH). Following DMH injections of 60 and 200 mg/kg, normal DNA synthesis was rapidly inhibited in all tissues. The greatest depressions were observed in the descending colon, followed closely by the ascending colon. DNA repair was estimated by measuring unscheduled DNA synthesis. No repair was observable in the descending or ascending colon. The esophagus, forestomach, jejunum, and ileum demonstrated significant amounts of DNA repair, while the duodenum and gastric stomach displayed nominal or insignificant amounts of repair. Repair DNA synthesis was inhibited by simultaneous administration of caffeine and DMH.

ISSN:0098-4108    

DOI:10.1080/15287398409530485

出版商:Taylor & Francis Group    

年代:1984

数据来源: Taylor

摘要:

The embryotoxicity and teratogenicity of methylhydrazine, 1,1‐dimethylhydrazine, and 1,2‐dimethylhydrazine were investigated with pregnant Fischer‐344 rats. The compounds were administered ip on d 6–75 of pregnancy. A dose‐dependent reduction in maternal weight gains occurred for all three compounds. A dose‐related teratogenic effect did not occur for any of the three compounds. Embryotoxicity, manifested as reduced 20‐d fetal weights, occurred only in the 1,1‐dimethylhydrazine and 7,2‐dimethylhydrazine high‐dose treatment groups. The results indicate that none of the three methylated hydrazine derivatives are selectively embryotoxic or teratogenic in the rat.

ISSN:0098-4108    

DOI:10.1080/15287398409530486

出版商:Taylor & Francis Group    

年代:1984

数据来源: Taylor