摘要:

The effects of short‐term exposure to ozone on control and elastase‐induced emphysematous rats were examined to investigate whether emphysema would change the pulmonary susceptibility to oxidant air pollution. Emphysema was induced in rats after a single intratracheal instillation of 0.2 IU elastase/g body weight. Histologically, panacinar emphysema was apparent at 2, 4, 8, and 76 wk, that is, the total duration of the experiment. The diagnosis was confirmed by morphometry: the mean linear intercepts (MLI) of elastase‐treated rats were significantly increased at all observation times, whereas the internal surface areas (ISA) of the elastase‐treated rats were significantly decreased. In addition, pulmonary function tests provided supportive evidence for the diagnosis of emphysema. Respiratory system compliance and functional residual capacity showed a significant increase in elastase‐treated rats. No differences in inspiratory capacity or in forced vital capacity between control rats and elastase‐treated rats were observed. The above data are indicative for a rat model for elastase‐induced emphysema. Short‐term exposure to ozone of elastase‐treated rats revealed panacinar emphysema, including an inflammatory response in the centroacinar region. No differences in MLI as well as in ISA between ozone‐exposed rats (with or without emphysema) and their respective controls were observed. Short‐term exposure to ozone induced an identical, significant increase in protein content, lactate dehydrogenase, glucose‐6‐phosphate dehydrogenase, and glutathione peroxidase activities in lungs of normal and emphysematous rats. Moreover, these results strongly suggest that emphysematous rats are not more susceptible to ozone than nonemphysematous rats.

ISSN:0098-4108    

DOI:10.1080/15287398909531230

出版商:Taylor & Francis Group    

年代:1989

数据来源: Taylor

摘要:

Although naturally occurring and mutant organisms, historically, have been released into the environment for various purposes, health concerns associated with the release of microorganisms have recently resurfaced. Federal agencies have been given the task of reassuring society that any released organisms are not likely to produce adverse health effects. Methods, therefore, for evaluating the potential health effects due to environmental release of mutant and genetically engineered microorganisms are under investigation. A mouse model was developed that examines morbidity, mortality, and more indirect effects such as colonization potential of the intestinal tract, as well as competition with and alteration of the intestinal microbiota populations. ThePseudomonasspp. used in this study were isolated from a commercial product and used for degrading polychlorinated biphenyls. Mice were dosed individually with 103, 106, and 109colony‐forming units of each microorganism. At specific time intervals the intestines were removed and examined for the presence of the dosed microorganism. At the two higher doses, 106and 109colony‐forming units,P. maltophiliastrain BC6 and twoP. aeruginosastrains, BC16 and BC18, were recoverable 48 h after dosing. The naturally occurringP. aeruginosastrain, PAMG, isolated from a mouse intestinal homogenate produced a similar response. Statistical analysis indicated that in some of the dosed animals, an alteration in the distribution of normal intestinal microflora occurred.Pseudomonas maltophiliastrain BC6 andP. aeruginosastrains BC16 and BC17 caused a change in the obligately anaerobic predominantly gram‐negative rod counts, andP. aeruginosastrain BC17 produced a dose effect on the total anaerobic count at the 10% confidence level. The total aerobic count was unaffected by the presence of the dosed pseudomonads.

ISSN:0098-4108    

DOI:10.1080/15287398909531231

出版商:Taylor & Francis Group    

年代:1989

数据来源: Taylor

摘要:

Male and female mice were treated subcutaneously (sc) with 1–100 ml/kg of di‐(2‐ethylhexyl) phthalate (DEHP) on d 1, 5, and 10 of the experiment and evaluated at d 21 for reproductive performance, selected biochemical parameters of the gonads, and histological alterations of the gonads. In both male and female treated mice there was a reduction in incidence of pregnancy. There were biochemical suggestions of reduced anabolic activity in the gonads (as reflected by decreased ATPase activity and of RNA, DNA, and protein content), and of increased catabolic activity in the gonads (as reflected by an increase in lysosomal enzyme activity and histological damage). Testicular, but not ovarian, weight was reduced in treated animals. Of the other parameters examined, the ovaries exhibited histological injury at lower doses of DEHP than the testes, but unlike testes, there was not a significant dose‐related increase in histopathology. Biochemical changes were dose‐related, for the most part, in both ovaries and testes, with the changes being more pronounced in testes. In general, reduced fertility appeared to be the most sensitive indicator for gonadotoxicity from DEHP, followed by biochemical changes and histological evidence of injury to the gonads.

ISSN:0098-4108    

DOI:10.1080/15287398909531232

出版商:Taylor & Francis Group    

年代:1989

数据来源: Taylor

摘要:

The development of organophosphorus‐induced delayed neurotoxicity (OPIDN) was studied in the European ferret (Mustela putorius furo). A single oral or dermal dose of 250, 500, or 1000 mg tri‐o‐tolyl phosphate (TOTP)/kg body weight was administered to adult male ferrets. Com oil served as the vehicle in the oral test and 95% ethanol was the vehicle in the dermal test. At 48 h posttreatment, half the animals in each group were killed by cervical dislocation for assessment of whole‐brain neuropathy target esterase (NTE) activity. The remaining 5 animals per group were observed and examined neurologically on a daily basis for a subsequent 54 d. All ferrets dosed dermally with 1000 mg TOTP/kg body weight developed clinical signs characteristic of OPIDN ranging from ataxia to partial paresis. Ferrets administered 250 and 500 mg TOTP/kg body weight via the dermal route displayed variable degrees of hind limb weakness and ataxia. Of the animals dosed orally, only those in the 1000 mg TOTP/kg body weight group showed clinical signs indicative of OPIDN. These signs did not progress beyond mild ataxia. Small amounts of axonal degeneration were noted in the dorsolateral part of the lateral funiculus and in the fasciculus gracilis of spinal cords in ferrets receiving dermal doses of 1000 mg TOTP/kg body weight. Whole‐brain neuropathy target esterase activity was also maximally inhibited (46%) in animals receiving 1000 mg TOTP/kg dermally. These results suggest that the ferret is a species that is susceptible to OPIDN.

ISSN:0098-4108    

DOI:10.1080/15287398909531233

出版商:Taylor & Francis Group    

年代:1989

数据来源: Taylor

摘要:

PurifiedAlternaria alternataaltertoxins I, II, and III were evaluated for comparative cytotoxicity and ability to inhibit gap junction communication in the Chinese hamster lung metabolic cooperation assay. The noncytotoxic test range for each altertoxin was determined for the metabolic communication assays: altertoxin I, 1, 2, 3, 4, 5 μg/ml; altertoxin II, 0.02, 0.008, 0.006, 0.004, 0.002, 0.0008 μg/ml; and altertoxin III, 0.2, 0.1, 0.08, 0.06, 0.04 μg/ml. Altertoxin II was the most cytoxic in the V79 system, followed by altertoxins III and I. The last cytotoxic of the three, altertoxin I, weakly disrupted metabolic communication at two concentrations (4 and 5 μg/ml). Altertoxins III and II did not significantly inhibit gap junction communication more than the weak tumor promoter 4‐O‐methyl ether tetradecanoylphorbol 13‐acetate.

ISSN:0098-4108    

DOI:10.1080/15287398909531234

出版商:Taylor & Francis Group    

年代:1989

数据来源: Taylor

摘要:

Isolated perfused liver and cultures of rat hepatocytes were assessed for the quantitative evaluation of hepatotoxicity. Release of de novo biosynthesized plasma proteins and acid hydrolases into perfusion or culture media was taken as an indication of the integrity of hepatocytes in both systems. The activities of six acid hydrolases, α‐L‐fucosidase, α‐D‐galactosidase, β‐D‐galactosidase, β‐D‐N‐acetylgalactosaminidase, β‐D‐N‐acetylglucos‐aminidase, and cathepsin D, were assayed in collagenase‐segregated hepatocytes and in monolayer cultures of rat liver cells obtained via collagenase perfusion of rat liver. In situ, liver perfusion with collagenase led to a loss of 45 ± 5% of the total acid hydrolase activity in the mitochondrial‐lysosomal pellet of the liver cells with concomitant increase of these enzymes in the cytosol. In monolayer cultures over a period of 30 h, increased activity of cathepsin D, β‐D‐galactosidase, and β‐D‐N‐acetylglucosaminidase in the mitochondrial‐lysosomal pellet and the cytosol fraction was evident with concurrent biosynthesis of plasma proteins. The use of radioactive tracing techniques with the isolated perfused liver revealed that the rate of catabolism of intracellular protein was ∼5 times that of plasma protein synthesis. Both methods described here are suitable for the study of the effects of toxins on the function of hepatocytes.

ISSN:0098-4108    

DOI:10.1080/15287398909531235

出版商:Taylor & Francis Group    

年代:1989

数据来源: Taylor

摘要:

Short‐term oral administration of unleaded gasoline to male rats reproduces the accumulation of phagolysosomes (hyaline droplets) in epithelial cells of the renal proximal convoluted tubules (PCT) observed following long‐term inhalation of wholly volatilized gasoline. Phagolysosomes are partially composed of α2u‐globulin, a low‐molecular‐weight protein, unique to male rats. In this study, dose‐dependent and chronologic alterations of phagolysosomes caused by gasoline were observed by transmission electron microscopy. Exposure to commercially available unleaded gasoline (0.4–2.0 ml/kg, po, once daily, 9 d) increased the number and size of phagolysosomes in epithelial cells of the PCX in male rat kidney. However, administration of 0.04 ml gasoline/kg or less was ineffective in inducing phagolysosomal accumulation. Sub‐cellular analysis revealed that many of the phagolysosomes observed in treated rats (doses greater than 0.4 ml/kg) were angular and had cross‐sectional diameters varying from 0.5 to 9 μm; in controls the majority of phagolysosomes were round and their diameter varied from 0.5 to 2.5 μm. Treatment of male rats with gasoline (2.0 ml/kg body weight, po, 1–9 d) caused a progressive increase in the number and size of phagolysosomes in PCX epithelial cells dependent on treatment duration. Alterations in phagolysosomal morphology and quantity occurred within 20 h following a single dose of gasoline, emphasizing that the process of phagolysosome accumulation is a dynamic phenomenon. Many of the enlarged phagolysosomes contained a condensed, crystalline core of greater electron density than the surrounding matrix. Furthermore, the rapid increase in abnormal, condensed contents in the phagolysosomes may indicate that a derangement of renal protein catabolism is the primary mechanism by which fuel hydrocarbons cause hyaline droplet nephropathy in male rats.

ISSN:0098-4108    

DOI:10.1080/15287398909531236

出版商:Taylor & Francis Group    

年代:1989

数据来源: Taylor

摘要:

Certain biochemical and behavioral effects of carbaryl were investigated in chicks. Six‐day‐old birds received 100 mg/kg body weight (bw) per day carbaryl for 7 d. Brain acetylcholinesterase (AChE) and neuropathy target esterase (NTE) were measured at 24 h after the first, third, and fifth dose during the 1 wk of treatment, and then at d 1, 3, 6, 10, 20, 30, and 40 after the last dose. Gait analysis was evaluated on each posttreatment day. No significant reduction in both NTE and AChE activities was noticed throughout the experiment. However, carbaryl altered the locomotion of the chicks from d 1 until d 40 after last treatment. The stride length of the treated birds was significantly shorter than that of the controls. A significant increase in the stride width and sine of the angle of placement was noticeable throughout the period of the experiment. Thus, treated chicks walked with abnormal gait. Delayed ataxia and paralysis occurred 20 d after the last treatment and lasted until the end of the experiment or eventually death.

ISSN:0098-4108    

DOI:10.1080/15287398909531237

出版商:Taylor & Francis Group    

年代:1989

数据来源: Taylor

ISSN:0098-4108    

DOI:10.1080/15287398909531238

出版商:Taylor & Francis Group    

年代:1989

数据来源: Taylor

ISSN:0098-4108    

DOI:10.1080/15287398909531229

出版商:Taylor & Francis Group    

年代:1989

数据来源: Taylor