Journal of toxicology and environmental health最新文献

{"title":"Biliary elimination of oral 2,4-dichlorophenoxyacetic acid and its metabolites in male and female Sprague-Dawley rats, B6C3F1 mice, and Syrian hamsters.","authors":"R J Griffin,&nbsp;J Salemme,&nbsp;J Clark,&nbsp;P Myers,&nbsp;L T Burka","doi":"10.1080/00984109708984033","DOIUrl":"https://doi.org/10.1080/00984109708984033","url":null,"abstract":"<p><p>The role of biliary elimination in the metabolic disposition of 2,4-D was evaluated in male and female Sprague-Dawley rats, B6C3F1 mice, and Syrian hamsters. Following cannulation of the bile duct, an intragastric (ig) dose of 2,4-D (200 mg/kg) was administered and bile was collected at 30- or 60-min intervals for up to 6 h. Bile flow rates were constant in rats, increased in mice, and decreased in hamsters throughout the collection periods. Total recovery of radioactivity was greatest in male mice (about 7% of administered dose over 4 h). Female mice and rats of both sexes excreted about 3% over the same interval and male and female hamsters about 1%. About 71-88% of the activity in bile was parent compound. The glycine conjugate of 2,4-D was found in bile from mice, rats, and hamsters and the taurine conjugate in bile from mice. The only sex-dependent difference in the metabolite profile was in mice. Male mice excreted twice as much glycine conjugate as female mice. An additional minor metabolite (4-7%) was present in rat and mouse bile. This was tentatively identified as 2,4-D-glucuronide based on its hydrolysis by beta-glucuronidase. One more very minor metabolite (3%) was detected in rat bile but was not characterized due to its lability. The results of this study indicate that there are species-dependent differences in the biliary elimination of 2,4-D but not sex-dependent differences.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 4","pages":"401-13"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20147923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ozone-induced DNA strand breaks In guinea pig tracheobronchial epithelial cells.","authors":"S F Ferng,&nbsp;C E Castro,&nbsp;A A Afifi,&nbsp;E Bermúdez,&nbsp;M G Mustafa","doi":"10.1080/00984109708984030","DOIUrl":"https://doi.org/10.1080/00984109708984030","url":null,"abstract":"<p><p>Ozone (O3), the major oxidant of photochemical smog, is thought to be genotoxic and a potential respiratory carcinogen or promoter of carcinogenic processes. Because of oxidative reactions with the mucus in the upper airway, O3 reaction products are able to penetrate into the tracheobronchial epithelial (TE) cells. The carcinogenic effects of O3 on the TE cells are especially of interest since most previous studies have focused on the morphology or permeability changes of tracheas only. Therefore, the objective of this study was to examine the potential O3 genotoxicity in TE cells after an in vivo exposure, using DNA strand breaks as an index. Two-month-old male Dunkin-Hartley guinea pigs, specific pathogen free, 4 in each group, were exposed to 1.0 ppm O3 for 0, 12, 24, 48, 72, or 96 h. Animals exposed to filtered air without O3 exposure were used as controls. After O3 exposure, the trachea with two main bronchi was removed from each animal, and TE cells were isolated and employed for determination of DNA strand breaks by fluorometric analysis of DNA unwinding (FADU). The statistical significance level was set at alpha = .05. Compared with controls, ozone exposure did not alter the TE cell yield or viability, but caused an increase in protein content in tracheal lavage and an increase in DNA strand breaks. The amount of DNA left in the alkali lysate of TE cells found at 72 h exposure was significantly decreased from controls for 3 different alkali incubation times. An increase of the double-stranded DNA left in the alkali lysate of TE cells was observed at 96 h of exposure and approached the value of 24 h of exposure. The same pattern was seen with all 3 different alkali incubation times at 15 degrees C. One Qd unit was estimated to correspond to 100 strand breaks per cell. The Qd was also used as an indicator for O3 damage. Compared to controls, the Qd increases significantly after 1 ppm O3 exposure for 72 h, regardless of the alkali incubation time at 15 degrees C.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 4","pages":"353-67"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20147920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential induction of polyamine oxidase activity in liver and heart of iron-overloaded rats.","authors":"U R Tipnis, G Y He, M F Khan","doi":"10.1080/00984109708984024","DOIUrl":"10.1080/00984109708984024","url":null,"abstract":"<p><p>The present study was undertaken to investigate the effect of iron dextran treatment on polyamine oxidase (PAO) activity, iron accumulation, and lipid peroxidation in livers and hearts of rats. PAO catalyzes oxidative deamination of polyamines, the cellular aliphatic cations. This reaction produces highly toxic hydrogen peroxide, 3-acetamidopropanal, and precursors of higher polyamines. The rats were given iron dextran daily for 7 d. In iron-dextran-treated rats, a marked increase in the hepatic level of iron was associated with enhanced lipid peroxidation and increased PAO activity. Though iron accumulation and lipid peroxidation in the iron-treated rats increased significantly in the heart, PAO activity remained unchanged. The paraffin sections of livers stained with Perls iron stain showed the presence of iron in macrophages and hepatocytes. The sections of hearts showed iron deposits only in macrophages, while myocytes showed no iron staining. These results show that although iron dextran treatment results in accumulation of iron in both liver and heart, it induces PAO activity only in liver. The significance of increased PAO activity in lipid peroxidation and fibrosis in iron-mediated injury is discussed.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 3","pages":"235-44"},"PeriodicalIF":0.0,"publicationDate":"1997-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20129509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of different degrees of reduced renal mass on the renal and hepatic disposition of administered cadmium.","authors":"R K Zalups","doi":"10.1080/00984109708984025","DOIUrl":"https://doi.org/10.1080/00984109708984025","url":null,"abstract":"<p><p>The present study was designed to evaluate, in rats, the effect of varying degrees of reduced renal mass on the disposition of administered cadmium. As part of this evaluation, the intrarenal, hepatic, and hematological disposition of cadmium and the urinary and fecal excretion of cadmium were studied and characterized in control, uninephrectomized (NPX), and 75% nephrectomized (75% NPX) rats 1 d, 2 d, and 7 d after the intravenous injection of a nonnephrotoxic 8.9 mumol/kg dose of cadmium chloride. Renal accumulation of cadmium, especially in the cortex and outer stripe of the outer medulla, was reduced significantly in the 75% NPX rats, but not in the NPX rats, between d 2 and 7 after the injection of cadmium. The diminution in the renal accumulation of cadmium in the 75% NPX rats was most likely due to diminished glomerular filtration rate and renal clearance of cadmium induced by 75% nephrectomy. Despite reduced glomerular filtration rate, the cumulative urinary excretion of cadmium in the 75% NPX rats was significantly greater than that in either the NPX rats or the control rats. It should be mentioned, however, that very little of the administered dose of cadmium was excreted in the urine by any of the three groups of rats. Interestingly, the content of cadmium in the liver was significantly greater in 75% NPX rats than in NPX or control rats between d 1 and 7 after the injection of cadmium. Moreover, the 75% NPX rats excreted significantly less cadmium in the feces over the 7 d of study than did the other 2 groups of rats, indicating that 75% nephrectomy causes a significant alteration in one or more of the mechanisms involved in the fecal excretion of cadmium. In summary, the findings from the present study indicate that the renal and hepatic handling of administered cadmium in rats changes significantly when renal mass is reduced by 75%. Further studies are needed to better characterize the effects of reductions of renal mass, which impair renal function significantly, on both the disposition and toxicity of cadmium in renal and hepatic tissues.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 3","pages":"245-64"},"PeriodicalIF":0.0,"publicationDate":"1997-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20129511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subchronic toxicity of 2,2',3,3',4,4'-hexachlorobiphenyl in rats.","authors":"P Lecavalier,&nbsp;I Chu,&nbsp;A Yagminas,&nbsp;D C Villeneuve,&nbsp;R Poon,&nbsp;M Feeley,&nbsp;H Håkansson,&nbsp;U G Ahlborg,&nbsp;V E Valli,&nbsp;A Bergman,&nbsp;R F Seegal,&nbsp;S W Kennedy","doi":"10.1080/00984109708984026","DOIUrl":"https://doi.org/10.1080/00984109708984026","url":null,"abstract":"<p><p>The subchronic toxicity of 2,2',3,3',4,4'-hexachlorobiphenyl (PCB 128) was investigated in rats following dietary exposure at 0, 0.05, 0.5, 5, or 50 ppm for 13 wk. The growth rate was not affected by treatment and no apparent clinical signs of toxicity were observed. There was a significant increase in liver weight in the 50 ppm females. The liver ethoxyresorufin deethylase (EROD) activity was increased by five- and fourfold in the highest dose males and females, respectively, while aminopyrine demethylase (ADPM) activity was significantly increased only in the highest dose females. Liver vitamin A was significantly reduced in the highest dose females. No other biochemical or hematological effects were observed. Treatment-related histopathological changes were seen in the thyroid and liver, and to a lesser extent in the bone marrow and thymus. Residue data showed a dose-dependent accumulation of PCB 128 in the following tissues: fat, liver, kidney, brain, spleen, and serum, with the highest concentration being found in fat followed by liver and kidney. Based on these data, the no-observable-adverse-effect level of PCB 128 was judged to be 0.5 ppm in diet or 42 micrograms/kg body weight.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 3","pages":"265-77"},"PeriodicalIF":0.0,"publicationDate":"1997-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20129955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of inducible nitric oxide synthase gene expression and lung inflammation following intratracheal instillation of silica, coal, carbonyl iron, or titanium dioxide in rats.","authors":"J A Blackford,&nbsp;W Jones,&nbsp;R D Dey,&nbsp;V Castranova","doi":"10.1080/00984109708984022","DOIUrl":"https://doi.org/10.1080/00984109708984022","url":null,"abstract":"<p><p>The pulmonary toxicity of the respirable dusts silica, coal, carbonyl iron, and titanium dioxide on alveolar macrophage (AM) and neutrophil (PMN) inducible nitric oxide synthase (iNOS) gene expression and nitric oxide (NO) production was investigated. Rats were intratracheally instilled with 5 mg/100 g body weight of silica, coal, carbonyl iron, or titanium dioxide. The dust particles averaged less than 5 microns in diameter. Bronchoalveolar lavage was performed 24 h later. Bronchoalveolar lavage cell (BALC) differentials, iNOS gene expression and NO production by BALC (measured indirectly as NO-dependent chemiluminescence), and lavageable lung protein levels were measured. Analyzed on an equal mass basis, silica, coal, and titanium dioxide dusts increased the production of iNOS-dependent NO by AM. Silica and titanium dioxide both increased the levels of iNOS mRNA while carbonyl iron and coal did not. Each dust caused an increase in PMN, indicating an inflammatory response. Carbonyl iron and titanium dioxide decreased the numbers of AM. Levels of acellular lavageable lung protein were increased by silica, carbonyl iron, and titanium dioxide. When exposure was normalized for an equal number of particles, the pneumotoxic dusts, silica and coal, caused more inflammation and NO production than the nuisance dusts, carbonyl iron and titanium dioxide. Therefore, it appears that particle number is a more appropriate metric of exposure than mass when comparing the relative pathogenicity of dusts of different sizes. Furthermore, since the potency of these dusts (on a particle number basis) to increase iNOS gene expression reflects their inflammatory and pathogenic potential, it is proposed that NO may contribute to the early inflammatory damage observed in the lung following dust exposure.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 3","pages":"203-18"},"PeriodicalIF":0.0,"publicationDate":"1997-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20129508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of dietary selenium on the disposition of arsenate in the female B6C3F1 mouse.","authors":"E M Kenyon,&nbsp;M F Hughes,&nbsp;O A Levander","doi":"10.1080/00984109708984027","DOIUrl":"https://doi.org/10.1080/00984109708984027","url":null,"abstract":"<p><p>Interactions between arsenic (As) and selenium (Se) at the metabolic level are multifaceted and complex. These interactions are of practical significance because populations in various parts of the world are simultaneously exposed to inorganic As in drinking water and Se mainly in the diet at varying levels. The primary goal of this study was to investigate whether differing dietary Se status would alter the profile of urinary metabolites or their time course for elimination after exposure to arsenate [As(V)]. Weanling female B6C3F1 mice were maintained for 28 d on either a control diet of powdered rodent meal sufficient in Se (A, 0.2 ppm) or Torula yeast-based (TYB) diets deficient (B, 0.02 ppm Se), sufficient (C, 0.2 ppm Se), or excessive (D, 2.0 ppm Se) in Se; mice then received by oral gavage 5 mg (As)/kg as sodium [73As] arsenate. The time course for elimination of total arsenic and metabolites in urine was measured over a 48-h period, and total arsenic was determined in feces and tissues at 48 h. Mice on the Se excess diet excreted a significantly higher percentage of urinary As as inorganic As, with a significantly decreased ratio of organic to inorganic As compared to Se-sufficient mice, suggesting that As methylation was decreased. Mice on the Se-deficient diet appeared to eliminate As(V), arsenite, and dimethylarsinic acid (DMA) in urine more slowly than Se-sufficient mice; however, further studies are required to confirm this finding. Mice on the Se-sufficient meal diet (A) excreted significantly less (by percent) arsenate-derived radioactivity in urine and more in feces compared to mice on the Se-sufficient TYB diet (C), with total elimination being similar for both groups. This indicates that mice on the meal diet absorbed significantly less As(V) than mice on the TYB diet, and this may be due to more fiber or \"bulk\" in the meal diet. This finding emphasizes the importance of considering dietary composition when interpreting and comparing As disposition studies. Overall this study provides suggestive evidence that dietary Se status alters As metabolism and disposition. This indicates that dietary Se status may be an issue that should be considered in the design and interpretation of epidemiologic studies.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 3","pages":"279-99"},"PeriodicalIF":0.0,"publicationDate":"1997-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20129513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic ultraviolet exposure-induced p53 gene alterations in Sencar mouse skin carcinogenesis model.","authors":"Y Tong,&nbsp;M A Smith,&nbsp;S B Tucker","doi":"10.1080/00984109708984023","DOIUrl":"https://doi.org/10.1080/00984109708984023","url":null,"abstract":"<p><p>Alterations of the tumor suppresser gene p53 have been found in ultraviolet radiation (UVR) related human skin cancers and in UVR-induced murine skin tumors. However, links between p53 gene alterations and the stages of carcinogenesis induced by UVR have not been clearly defined. We established a chronic UVR exposure-induced Sencar mouse skin carcinogenesis model to determine the frequency of p53 gene alterations in different stages of carcinogenesis, including UV-exposed skin, papillomas, squamous-cell carcinomas (SCCs), and malignant spindle-cell tumors (SCTs). A high incidence of SCCs and SCTs were found in this model. Positive p53 nuclear staining was found in 10/37 (27%) of SCCs and 12/24 (50%) of SCTs, but was not detected in normal skin or papillomas. DNA was isolated from 40 paraffin-embedded normal skin, UV-exposed skin, and tumor sections. The p53 gene (exons 5 and 6) was amplified from the sections by using nested polymerase chain reaction (PCR). Subsequent single-strand conformation polymorphism (SSCP) assay and sequencing analysis revealed one point mutation in exon 6 (coden 193, C-->A transition) from a UV-exposed skin sample, and seven point mutations in exon 5 (codens 146, 158, 150, 165, and 161, three C-->T, two C-->A, one C-->G, and one A-->T transition, respectively) from four SCTs, two SCCs and one UV-exposed skin sample. These experimental results demonstrate that alterations in the p53 gene are frequent events in chronic UV exposure-induced SCCs and later stage SCTs in Sencar mouse skin.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 3","pages":"219-34"},"PeriodicalIF":0.0,"publicationDate":"1997-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20129507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of malathion metabolites on degranulation of and mediator release by human and rat basophilic cells.","authors":"S Xiong,&nbsp;K Rodgers","doi":"10.1080/00984109708984019","DOIUrl":"https://doi.org/10.1080/00984109708984019","url":null,"abstract":"<p><p>In the present study, the effects of malathion and malathion derivatives on histamine and beta-hexosaminidase release by RBL-1 cells, rat peritoneal mast cells (RPMC), and human peripheral blood basophils (HPBB) and cutaneous mast calls were examined. One hour of incubation of RBL-1 cells with all organophosphate compounds tested, except for malathion and malathion monoacid, led to an increase in histamine release. beta-Hexosaminidase, an enzyme released by basophilic cells and a biochemical marker of degranulation, was not released from RBL-1 cells after 1 h of exposure to organophosphate compounds. Within 4 h, all compounds tested increased the release of histamine and beta-hexosaminidase. Longer exposures led to a decrease in the concentration of the compound that was required to cause mediator release. Exposure of RPMC to organophosphate compounds, with the exception of malathion monoacid and malathion (30 min) or malathion monoacid (1 h), led to the release of histamine, but not beta-hexosaminidase. Incubation of HPBB with malaoxon (51.4 +/- 2.8% total histamine released), malathion diacid (25.7 +/- 2.9%), beta-malathion monoacid (31.4 +/- 2.8%), and isomalathion (57.1 +/- 17.1%) for 1 h led to the release of histamine. Only malaoxon and isomalathion caused beta-hexosaminidase release from HPBB after a 1-h incubation. Incubation of cutaneous mast cells with malaoxon and beta-monoacid for 4 h led to increased release of histamine and beta-hexosaminidase at levels comparable to compound 48/80. These data suggest that malathion metabolites can cause rapid release of histamine from basophilic cells from a variety of origins and species. With prolonged incubation, malathion itself caused the release of mast-cell mediators, suggesting that the cells may be capable of metabolizing malathion. These data also indicate a disparity between the release kinetics of two different mast-cell mediators contained in granules by organophosphates, and that there are different mechanisms of mediator release.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 2","pages":"159-75"},"PeriodicalIF":0.0,"publicationDate":"1997-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20123592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioavailability of TNT residues in composts of TNT-contaminated soil.","authors":"W G Palmer,&nbsp;J R Beaman,&nbsp;D M Walters,&nbsp;D A Creasia","doi":"10.1080/00984109708984014","DOIUrl":"https://doi.org/10.1080/00984109708984014","url":null,"abstract":"<p><p>Composting is being explored as a means to remediate 2,4,6-trinitrotoluene (TNT) contaminated soils. This process appears to modify TNT and to bind it to organic matter. The health hazards associated with dusts generated from such materials cannot be predicted without knowing if the association between TNT residues and compost particulate is stable in biological systems. To address this question, single doses of [14C]-TNT, soil spiked with [14C]-TNT, or compost generated with [14C]-TNT-spiked soils were administered to rats by intratracheal instillation. The appearance of 14C in urine and tissues was taken as an indication of the bioavailability of TNT residues from compost particles. In rats instilled with neat [14C]-TNT, about 35% of the 14C dose appeared in urine within 3 d. The 14C excreted in urine by these rats decreased rapidly thereafter, and was undetectable by 4 wk after treatment. Similar results were obtained with soil-treated rats. In contrast, after treatment with [14C]-TNT-labeled compost, only 2.3% of the total 14C dose appeared in urine during the first 3 d. Low levels of 14C continued to be excreted in urine from compost-treated rats for more than 6 mo, and the total amount of 14C in urine was comparable to that in TNT-treated animals. Determination of the radiolabel in tissues showed that 14C accumulated in the kidneys of rats treated with labeled compost but not in rats treated with [14C]-TNT or [14C]-TNT-spiked soil. These results indicate that the association between TNT and particulate matter in compost is not stable when introduced into the lungs. Accumulation of 14C in kidneys suggests the presence of a unique TNT residue in compost-treated rats. The rate of excretion and tissue disposition of 14C in rats treated with TNT-spiked soil indicate that TNT in soil is freely available in the lungs.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 2","pages":"97-108"},"PeriodicalIF":0.0,"publicationDate":"1997-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20122520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}