摘要:

The cancer mortality experience of 2649 Swedish grain millers was followed during the period from 1961 to 1979. Although the overall cancer incidence was not elevated, the risk of primary liver cancer was significantly elevated for this group (standard incidence ratio ‐ 238). The Swedish data is compared to the cancer mortality experience of workers in the Netherlands and the United States who are also involved in the bulk handling and storage of agricultural foodstuffs (e.g., peanuts, grains). The varying occupational exposures in this international comparison help establish etiologic hypotheses in the absence of comprehensive exposure information. Agents of potential concern include metabolic products of fungal contaminants (e.g., aflatoxins) and pesticides used to protect grain from insect infestation.

ISSN:0098-4108    

DOI:10.1080/15287398709531068

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

To evaluate a critical concentration concept of cadmium (Cd) toxicity on the kidney, relationships of renal Cd level with urinary excretion of various substances—i.e., me‐tallothionein, alkaline phosphatase, lactate dehydrogenase, N‐acefyl‐β‐D‐glucosa‐minidase, total protein, Cd, copper, and zinc—were studied in Cd‐injected rats. At the renal Cd concentration of 100–200 μg/g tissue, a dramatic increase of all these substances in urine was observed, supporting the idea of the critical concentration proposed by Friberg and co‐workers (1974). The significance of increase of urinary metallothionein below this level is also discussed.

ISSN:0098-4108    

DOI:10.1080/15287398709531069

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

The administration of sodium N‐methyl‐N‐dithiocarboxy‐D‐glucamine (NaC) at 500 mg/kg, i.p., or sodium calcium diethylenetriaminepentaacetic acid (DTPA) at 632.5 mg/kg, i.p., reduces the serum enzyme levels characteristic of hepatic damage following the intravenous administration of cadmium chloride (3.5 mg CdCl2• 2.5H2Ol kg). Some effect on serum enzyme levels was found even when the interval between administration of cadmium chloride and that of the antagonist was as great as 4 h. The enzymes examined included aspartate aminotransferase (AST), γ‐glutamyl transpeptidase (GGT), alanine aminotransferase (SGPT), and alkaline phosphatase (AP). A histopathological examination of the livers of such animals also reveals the presence of a significant protective action.

ISSN:0098-4108    

DOI:10.1080/15287398709531070

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

To establish the chemical composition of the arsenic inclusion, freshly isolated preparations of inclusions and eponembedded thin sections of inclusions were subjected to ultrastructural cytochemical analysis. Intranuclear inclusions are composed of amorphous, arsenic‐containing subunits aligned linearly to form a coiled complex. Lipase, ribonuclease, deoxyribonuclease, trypsin, pepsin, protease, amylase, or eth‐ylenediaminetetraacetic acid (EDTA) was used to digest or chelate these inclusions. Following enzymatic digestion or chelation, the electron opacity of inclusions was compared with that of control sections exposed for equal times to equivalent solutions lacking the enzymes. Exposure to amylase caused a consistent reduction in the electron opacity of thin sections of inclusions and almost complete digestion of the freshly isolated preparations of inclusions. This was indicative of the presence of a carbohydrate moiety within arsenic inclusions. Incubation of inclusions with EDTA resulted in solubilization of freshly isolated and thin‐sectioned embedded material. These data indicated that the intranuclear arsenic inclusion is composed of both metallic and carbohydrate moieties, confirming earlier studies which identified arsenic within inclusions using instrumental neutron activation analysis and X‐ray microprobe analysis.

ISSN:0098-4108    

DOI:10.1080/15287398709531071

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

Activities of enzymes responsible for the maintenance of reduced glutathione (GSH) levels have been shown in a previous study to be increased in rat lungs following a 3‐h exposure to cadmium oxide aerosols at 5.0 mg/m3. In this study, the ability of the lung to maintain levels of CSH during challenge with tertbutyl hydroperoxide (tBuOOH) was evaluated in isolated perfused lungs from control and cadmium oxide‐exposed rats. Changes in glutathione redox status were indicated by measurements of nonprotein sulfhydryls (NPSH), total glutathione CA CSH + GSSG), and glutathione disulfide (GSSG) in liquid nitrogen freeze‐clamped lungs after 3‐min infusions with 0–0.6 mM tBuOOH. In control and cadmium oxide‐exposed lungs, levels of ½ GSH + GSSG remained constant over the range of 0–0.6 mM tBuOOH, indicating that no loss of glutathione from the system had occurred. In experiments with control lungs, levels of NPSH fell from 8.04 ± 0.22 to 3.09 ± 0.40 μmol/g dry weight when tBuOOH concentrations were increased from 0 to 0.6 mM (n = 20–23). In cadmium oxide‐exposed lungs, NPSH levels also decreased proportionally to increases in CSSC. However, at concentrations of 0.075 and 0.15 mM tBuOOH, significantly smaller decreases in NPSH levels were observed in cadmium oxide‐exposed lungs compared with controls. This protection against the CSH‐depleting effects of tBuOOH might be explained by increased tissue levels of CSH‐related enzymes.

ISSN:0098-4108    

DOI:10.1080/15287398709531072

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

Rabbits were exposed (2h/d) to atmospheres consisting of 0.5 mglrn3(0.3 μm) H2SOAplus NO2at either 0.3 (low) or 1 ppm (high). Animals were sacrificed 24 h after 2, 6, or 13 exposures, and cells were recovered from the lungs by bronchopulmonary lavage. Exposure to high NO2with acid resulted in an increase in neutrophils at all time points and an increase in phagocytic capacity of macrophages after two or six exposures. On the other hand, exposure to the low NO2with acid resulted in depressed phagocytic capacity and mobility. The results were compared with those for NO2or H2SO4given alone.

ISSN:0098-4108    

DOI:10.1080/15287398709531073

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

In the current study, biochemical measures of lipid peroxidation following 4‐h inhalation exposure to 76 mg/m3(40 ppm) nitrogen dioxide were correlated with measures of deposition and tissue antioxidant levels in the nasal cavity and the trachea of the Fischer rat. In addition, respiratory‐tract mucus samples were collected via esopha‐geal cannulation and nasopharyngeal lavage over known time periods, and were analyzed for phospholipid (PL) content to provide an index of the unsaturated lipids (UL) that they may contain. UL are thought to be important in the scavenging of oxidants by the mucous lining layer. Nasal deposition efficiency, as measured in the surgically isolated upper respiratory tract under unidirectional flow conditions, averaged 25%, corresponding to an absolute deposition rate of 41 nmol/min. Vitamin E levels averaged 1.7, 5.9, and 0.7 nmol/μmol PL in nasal, tracheal, and pulmonary tissues, respectively. The level in the trachea was significantly (p < 0.005) higher than in the other tissues. As estimated from the increase in lavage PL content over 1 h, the overall mucous PL transport rate was less than 0.013 nmol/min, suggesting the PL of the mucous lining layer could not offer significant protection against the inhaled NO2. Conjugated dienes were detected in two of four pooled nasal tissue samples. Thio‐barbituric acid‐reactive material levels in tracheal tissues were significantly elevated over control levels by NO2(p < 0.05). Thus, despite the relatively high vitamin E levels, 4‐h NO2exposure appeared to result in lipid peroxidation in the trachea and, perhaps, in the nasal airways of the rat, a result that correlated with the apparent lack of oxidant‐scavenging species in the mucus lining these airways.

ISSN:0098-4108    

DOI:10.1080/15287398709531074

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

In order to evaluate the early response of the alveolar epithelium following lung injury, male Long‐Evans adult rats (280–350 g) were treated with a single dose (30 mg/kg, ip) of the herbicide paraquat. No animal died during the 72 h that followed the acute administration of the herbicide. When compared to control, total lipid, phosphatidylcholine, and disaturated phosphatidylcholine contents of lung homoge‐nates from the paraquat‐treated rats were significantly reduced 48 h postdose (respectively 70, 24, and 37%). Comparatively, the total lung alkaline phosphatase activity was significantly reduced as early as 12 h postdose, and by 48 h the activity had decreased by ∼50%. Although a significant decrease in total lung acid phosphatase activity was observed 24 and 48 h after the treatment, the effect was much less than with the alkaline phosphatase activity (15% versus 50%, respectively). The lysosomal β‐N‐acetytglucosaminidase and the cytoplasmic lactate dehydrogenase activities were not affected by the herbicide treatment. A subcellular fractionation of the treated lungs showed that 48 h postdose, the total alkaline phosphatase activities associated with lamellar body and surfactant fractions were decreased respectively by 60% and 49%. Due to the intrinsic association of a strong alkaline phosphatase activity with the pulmonary surfactant system, these data suggest that the monitoring of the alkaline phosphatase activity in lung fractions could represent an early and sensitive indicator of toxicity to the alveolar epithelium, most probably to type II cells.

ISSN:0098-4108    

DOI:10.1080/15287398709531075

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

The metabolism of three tetrachlorobenzene isomers (TeCB) was investigated in the squirrel monkey. The animals were administered orally 6 single doses of14C‐labeled 1,2,3,4‐, 1,2,4,5‐, or 1,2,3,5‐tetrachlorobenzene over a 3‐wk period at levels ranging from 50 to 100 mg/kg body weight (b.w.) and kept in individual metabolism cages to collect urine and feces for radioassay. Approximately 38% (1,2,3,4‐TeCB), 36% (1,2,3,5‐TeCB), and 18% (1,2,4,5‐TeCB) of the doses were excreted respectively in the feces 48 h postadministration. In monkeys dosed with 1,2,3,4‐TeCB, unchanged compound accounted for 50% of the fecal radioactivity; its fecal metabolites were identified as 1,2,4,5‐tetrachlorophenol (TeCP, 22%), U‐acetyl‐S‐(2,3,4,5‐tetrachloro‐phenyl) cysteine (18%), 2,3,4,5‐tetrachlorophenyl sulfinic acid (3%), 2,3,4‐trichloro‐phenyl methyl sulfide (0.6%), and 2,3,4,5‐tetrachlorophenyl methyl sulfide (0.2%). As was the case with 1,2,3,4‐TeCB, unchanged compound accounted for more than 50% of the fecal radioactivity found in the monkeys dosed with 1,2,3,5‐TeCB. The fecal metabolites of 1,2,3,5‐TeCB consisted of 2,3,4,5‐TeCP (2%), 2,3,4,6‐TeCP (14%), 2,3,5,6‐TeCP (9%), and 2,3,5,6‐tetrachlorophenyl sulfinic acid (15%). No metabolites were detected in the feces of monkeys dosed with 1,2,4,5‐TeCB. While the fecal route represented the major route of excretion for 1,2,3,4‐TeCB, the other two isomers were eliminated exclusively in the feces. The above data in the squirrel monkey are different from those obtained with the rat and the rabbit, and demonstrate the different metabolic pathways for the isomers.

ISSN:0098-4108    

DOI:10.1080/15287398709531076

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

Female BALB/c and B6C3F1mice were examined after a 3‐wk exposure to dietary estradiol (0, 400, 800, 1600, and 3200 ppb) in a purified (AIN‐76A) or a natural‐ingredient (NIH‐07) diet. The use of AIN‐76A was associated with a 9–13% greater (p < 0.001) body weight and a 36–43% higher (p < 0.001) serum cholesterol in both mouse genotypes when compared to mice fed NIH‐07. Conversely, when fed NIH‐07, both mouse genotypes had a 20–22% higher (p < 0.003) serum urea nitogren and 2–3.5% higher erythrocyte count (p < 0.001) and hemoglobin concentration (p < 0.04) than when fed AIN‐76A. Reduced erythrocyte parameters suggest that chronic feeding of the purified diet might result in anemia. No significant compound or diet‐related differences were noted for serum creatinine, alanine aminotransferase, aspartate aminotransferase, or gamma‐glutamyl transferase. Although there was no diet effect on absolute or differential white blood cell count, estradiol caused a decrease in the total white blood cell count (p < 0.014) and an increase in the percentage of poly‐morphonuclear leukocytes (p < 0.014) in BALB/c and decreased the percentage of lymphocytes (p < 0.005) in B6C3F1, females. In addition, estradiol increased uterine weight and inhibited thymic and splenic weights in one or both genotypes. Spleen and thymus weight responses to estradiol were not significantly influenced by diet. However, the uterine weight responses to estradiol were apparently influenced by diet in both genotypes. In B6C3F1mice, the uterus weighed more at each level of estradiol when mice were fed AIN‐76A compared to NIH‐07 diet. In BALB/c mice, this was true only at the two lower dietary concentrations of estradiol. In conclusion, mice fed the purified diet, AIN‐76A, differed from those fed the cereal‐based diet, NIH‐07, in hematology, clinical chemistry, and uterine weight response to estradiol.

ISSN:0098-4108    

DOI:10.1080/15287398709531077

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor