摘要:

The effects of polychlorinated biphenyls (PCBs) on the development of several intestinal and serum marker enzymes have been studied. The three congeners 4‐monochloro (1‐CB), 3,4,3’,4'‐tetrachloro (4‐CB), and 2,4,5,2’,4’,5'‐hexachloro (6‐CB) biphenyl were administered orally to pregnant rats on d 8, 11, 13, 15, and 18 of gestation. 1‐CB and 6‐CB were intubated at doses of 30 mg/kg·d (total dose, 150 mg/kg) and 4‐CB was administered at 3 mg/kg·d (total dose, 15 mg/kg). Levels of intestinal alkaline phosphatase, monoamine ioxidase, and Na+,K+‐adenosin‐5'‐etriphosphatase and levels of serum alkaline phosphatase, sorbitol dehydrogenase, and ß‐hydroxybutyrate dehydrogenase were measured in the dams after weaning and in their offspring at —1, 6, 20, and 55 d of age. Intestinal alkaline phosphatase activity was elevated at the later postnatal stages in the 1‐CB group and depressed at 55 d in the 4‐CB group, whereas serum alkaline phosphatase levels were markedly depressed prenatally and postnatally in the 4‐CB and 6‐CB groups, respectively. Intestinal monoamine oxidase levels were markedly increased in the 6‐CB group at —1, 6, and 20 d of age and significantly depressed in the 4‐CB animals at —1 and 55 d of age. There was an increase in monoamine oxidase activity in the 4‐CB group at 6 d. The 1‐CB group exhibited depression of monoamine oxidase levels at 6 d and elevation at 20 and 55 d. Intestinal Na+,K+‐A TPase levels were elevated throughout development in the 1‐CB animals and at —1 and 6 d in the 4‐CB group. The 6‐CB animals showed elevated levels of Na+,K+‐A TPase only at 6 d. Serum ß‐hydroxybutyrate dehydrogenase and sorbitol dehydrogenase were induced prenatally in the 4‐CB animals but enzyme activities decreased to normal by 55 d of age. Significant depression of activity was evident in the 1‐CB and 6‐CB groups at —1 d in both enzymes.

ISSN:0098-4108    

DOI:10.1080/15287398209530137

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Body weight gain and hepatic concentrations of vitamin A were reduced in Sprague‐Dawley rats by pre‐ and postnatal exposure to 100 ppm polybrominated biphenyls (PBBs). The ratio of liver weight to body weight, activity of hepatic δ‐aminolevulinic acid (ALA) synthetase, and urinary excretion of uro‐ and coproporphyrins were increased by PBBs. Treatment with PBBs also increased the left atrial inotropic response to calcium. However, PBBs had no effect on development of the adrenergic neuronal transport system in heart, left atrial baselike peak tension, or inotropic response to ouabain. Thus PBBs retarded body weight gain and produced a variety of alterations in liver, but had little effect on cardiac contractile function.

ISSN:0098-4108    

DOI:10.1080/15287398209530138

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Exposure to polybrominated biphenyls (PBBs) resulted in increased activity of microsomal arylhydrocarbon hydroxylase and ethoxyresorufin‐O‐deethylase in rat lung. Clearance of 5‐hydroxytryptamine (5‐HT) and angiotensin I by perfused lungs was decreased by PBBs. However, PBBs had no effect on the activity of epoxide hydrolase, monoamine oxidase, or angiotensin‐converting enzyme in lung. The only histopathologic change detected in lungs from PBB‐treated rats was an increase in alveolar type II cell lamellar bodies. Selective accumulation of certain PBB congeners by lung was not observed in this investigation.

ISSN:0098-4108    

DOI:10.1080/15287398209530139

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

The intestinal uptake site, enterohepatic circulation, and excretion into bile, feces, and urine of alkyltins (tetra‐ and trialkyltin) were investigated after oral, sc, or intestinal administration of the compounds to rats and rabbits. Assays of tetra‐ and trialkyltins in biological materials were carried out by gas chromatography. The main uptake sites in the small intestine were the jejunum and duodenum for tetraalkyltins and the ileum and jejunum for trialkyltins. Tetra‐ and trialkyltins were detected in the small intestine and contents of the intestinal lumen after sc injection of these compounds in rats. These facts suggest that tetra‐ and trialkyltins are transported in the body through enterohepatic circulation. The route, rate, and amount of excretion of tetra‐and trialkyltins seem to depend on the velocity of dealkylation, doses, physical and chemical properties, and route of administration of the compounds.

ISSN:0098-4108    

DOI:10.1080/15287398209530140

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Maternal exposure to Cd reduces lung weight and alters pulmonary surfactant accumulation in the fetus. This may lead to respiratory distress and death postnatally. In this study, the effects of maternal Cd administration on additional biochemical parameters of the fetal lung were investigated. Pregnant rats were given sc injections of 8 mg/kg CdCl2on d 12–15 of gestation and sacrificed throughout late gestation. Fetal lungs were examined for protein, DNA, and glycogen. Incorporation of choline into total and disaturated phosphatidylcholine and sphingomyelin were measured in fetal lung slices. The DNA content of the treated lungs was reduced, but the protein/DNA ratio was not altered. Thus the reduced lung weight was due to hypoplasia, not hypotrophy. Incorporation of choline into pulmonary sphingomyelin was not altered by the treatment. Choline incorporation into both total and disaturated phosphatidylcholine, the most important surfactant component, was reduced on the final days of gestation. Glycogen was reduced in both absolute quantity and cellular concentration in lungs of treated fetuses. Glucose derived from glycogen is a major metabolic substrate in the fetal lung and probably contributes greatly to phospholipid synthesis. The reduction in glucose concentration in lungs of treated fetuses may be a factor in the diminished synthesis of pulmonary surfactant phosphatidylcholine before birth. Prenatal Cd exposure (1) causes pulmonary hypoplasia, (2) reduces the amount of glycogen present in the fetal lung, and (3) diminishes the rate of synthesis of pulmonary surfactant phosphatidylcholine.

ISSN:0098-4108    

DOI:10.1080/15287398209530141

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

The metabolism of 2‐acetylaminofluorene (AAF)in vitroand the urinary excretion of a single ip dose of AAF were studied in weanling rats maintained on an Se‐deficient diet or the same diet supplemented with 0.5 ppm Se. Hepatic microsomes isolated from Se‐supplemented rats generated greater amounts of noncarcinogenic phenolic metabolites of AAF than did microsomes from Se‐deficient animals. Under the same conditions, the production of the proximate carcinogenic metaboliteN‐hydroxy‐AAF was very low and no difference was detected between the two groups of rats. Microsomes from Se‐deficient rats exhibited moderately higher glucuronyltransferase activity. However, no difference was found between the two dietary groups with respect to hepatic soluble sulfotransferase activity.

ISSN:0098-4108    

DOI:10.1080/15287398209530142

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Lead accumulation was studied in rats treated with Pb through the dam's milk from birth to weaning. Dams of experimental litters received lead acetate in drinking water, while dams of control litters received a sodium acetate solution. Fluid consumption by dams and pup weight were monitored daily. No differences were seen in the dams’ fluid consumption or in mortality or growth rate of pups. Rats were sacrificed after 5, 10, 16, or 21 d of Pb treatment, or 3 and 3.5 mo after weaning. Samples of heart, brain, liver, kidney, intestine, and bone were solubilized in concentration nitric acid and analyzed for Pb by atomic absorption spectrophotometry. Nitric acid digests of blood samples from pups 10 and 21 d old and from animals allowed a Pb‐free period of 3–3.5 mo after treatment were also analyzed for Pb concentration. Levels of Pb in all tissues analyzed progressively increased during the first 10 d of treatment. After the Pb‐free period only bone Pb concentrations remained elevated. The results indicate that treatment of lactating dams is an efficient method of producing chronic Pb exposure of rat pups. The results also provide a means of comparing studies of Pb toxicity in which different treatment paradigms are used.

ISSN:0098-4108    

DOI:10.1080/15287398209530143

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Pregnant outbred albino rats (CD) and mice (CD‐1) were given epichlorohydrin by gastric intubation on d 6–15 of gestation. The rats were killed on d 21 (d 18 for mice) and the offspring checked for gross, visceral, and skeletal malformations. Epichlorohydrin caused a significant reduction in the weight gain of pregnant rats at 80 mg/kg·d as compared with the control group treated only with the vehicle. However, there was no evidence of teratogenicity in the rat fetuses even at a dose level (160 mg/kg·d) that caused the death of some of the treated dams. Epichlorohydrin also did not produce a statistically significant increase in the average percent of malformed mouse fetuses, even at 160 mg/kg·d, a dose that killed 3 of 32 treated dams. The 120 and 160 mg/kg·d levels did cause a significant (p < 0.05) reduction in the average fetal weight as compared with controls. In addition, the 120 mg/kg·d dose produced a statistically significant increase in the liver weight of the pregnant mouse. These observations indicate that the 120 and 160 mg/kg·d dose levels were toxic toward the dams and their unborn offspring. In a similar mouse study, glycidol showed no evidence of teratogenicity. There was a significant increase in the number of stunted fetuses at 200 mg/kg·d, but all of these were present in a single litter. Further, the same dose killed 5 of 30 dams.

ISSN:0098-4108    

DOI:10.1080/15287398209530144

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Pregnant outbred albino (CD‐1) mice received (gavage, three times a day in cottonseed oil) a xylene mixture (60.2%m‐xylene, 9.1%o‐xylene, 13.6%p‐xylene, and 17.0% ethyl benzene) on d 6–75 of gestation (d 1 being the day vaginal plugs were observed). The mice were killed on d 18, the general and reproductive health of the dams evaluated, and the fetuses examined and processed to characterize external, visceral, and skeletal malformations. At 3.6 ml/kg·d, xylene killed 12 of 38 dams and caused a significantly (p< 0.05) smaller average weight gain during pregnancy than did the vehicle (cottonseed oil). Fetuses from dams treated with xylene at 2.4 ml/kg·d and higher doses had average fetal weights significantly lower than that of the control fetuses. However, the percent of resorptions for xylene was significantly greater than for the control only at 3.6 ml/kg·d. At 2.4, 3.0, and 3.6 ml/kg·d xylene produced a significantly (p < 0.07) greater average percent of malformed fetuses than did the control. Cleft palate was the major malformation at all three doses. When bilateral (multiple) wavy ribs were counted as a malformation, the average percent of malformed fetuses increased from 7.8 to 10.5 at 3.0 ml/kg·d and from 9.1 to 73.4 at 3.6 ml/kg·d. It is concluded that xylene (mixed homers) is teratogenic to the CD‐1 mouse at 2.4 and 3.0 ml/kg·d, doses approaching lethal levels.

ISSN:0098-4108    

DOI:10.1080/15287398209530145

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

The preferential distribution of the relatively nonpolar pesticide chlordecone (CD) to liver rather than to fat tissues in humans suggests that it may be transported in plasma differently from other organochlorine pesticides. The plasma binding of [14C]CD was investigatedin vitroin human, rat, and pig plasma andin vivoin rat plasma. Protein and lipoprotein fractions were separated by serial ultracentrifugation. Heparin‐manganese precipitation and agorose gel electrophoresis were also carried out to determine whether separation techniques altered CD binding to plasma components.

ISSN:0098-4108    

DOI:10.1080/15287398209530146

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor