摘要:

Exposure of rats to hyperoxia (100% oxygen (or 64 h) resulted in striking alterations in the properties of samples obtained by bronchoalveolar lavage. The yield of neutrophils, lymphocytes, and red blood cells was increased, while the number of harvested alveolar macrophages decreased. The acellular lavage fluid level of protein was elevated, indicating lung damage. However, acellular phospholipid levels were unchanged. The ability of alveolar macrophages to produce reactive forms of oxygen in response to zymosan was significantly decreased by oxygen exposure. This impaired function was not fully explained by a decrease in viability of these phagocytes. In contrast, stimulant‐induced chemiluminescence was elevated after hyperoxia. This rise was not due to a change in cellular antioxidant levels or to a discernible increase in arachidonic acid metabolites. However, it was associated with increased cellular lipid peroxidation.

ISSN:0098-4108    

DOI:10.1080/15287399309531772

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

Using full‐factorial design experiments for three variables at two levels each and center replicates, we examined the effects of common agricultural carbamate insecticides, aldicarb and methomyl, and a triazine herbicide, metribuzin, on hormone levels in Sprague‐Dawley rats. Fifty‐four female rats were sampled at 2 and 6 wk during a 6‐wk exposure to individual chemicals or to combinations of them. Some main effects and interaction effects were significant. For example, rats treated with the herbicide (metribuzin) were hyperthyroid. The interactions of all three chemicals also significantly increased thyroxine levels. One year later, we repeated these experiments for 16 wk using 54 mate rats; the results were very similar. Metribuzin alone significantly increased thyroxine throughout the second study (at 7, 13, and 16 wk). Somatotropin levels were significantly altered after 13 wk of exposure. The same concentrations and mixtures of these three pesticides have now been shown to be implicated in learning impairment and other neurological functions, immune parameter changes, and endocrine changes. These findings support the concept of the interconnectedness of the nervous, endocrine, and immune systems and raise the likelihood of impacts on all three systems if one is shown to be affected. Development, growth, and reproduction all depend on the proper function of these three systems. These results strongly suggest the need to reassess currently allowed “safe” levels of chemicals based on adult dosages that are accepted in ground‐water and in our food supplies.

ISSN:0098-4108    

DOI:10.1080/15287399309531773

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

Mercer et al. (1977) proposed a three‐phase experimental design to establish withdrawal times, based on plasma pharmacokinetics. This approach was the premise of a study in which plasma pharmacokinetics and tissue depletion data of oxytetracycline after intramuscular administration were correlated. Correlations between estimated and measured concentrations were shown to be significant for kidney tissue (r = .9236, p < .001), liver tissue (r = .9302, p < .01) as well as for muscle tissue (r = .9045, p < .001). The data presented support the pharmacokinetic approach as proposed by Mercer et al. (1977) and demonstrate that tissue elimination rates correlate highly with elimination rates in plasma. Although generalizations must be applied with caution, this article shows that when certain criteria are fulfilled, plasma pharmacokinetics can reliably predict tissue withdrawal times.

ISSN:0098-4108    

DOI:10.1080/15287399309531774

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

Porphyrin patterns in avian and mammalian tissues and/or excreta have been proposed as qualitative and quantitative biomarkers of exposure to polyhalogenated hydrocarbons, heavy metals, and other environmental contaminants. However, no widely distributed terrestrial species has been characterized as a suitable model in which to assess porphyrin profiles in the evaluation of environmental contaminant exposure. The European starling, whose nests can be readily established and manipulated on contaminated sites, has many qualities that accommodate controlled field research and that suggest its suitability for such assessments. In the present studies, we measured the total and individual porphyrin concentrations in liver, kidney, and fecal‐urate excreta of nestling starlings from a nonconfaminated field site from day of hatch through d 17 of the nestling period. Total as well as individual 8‐, 7‐, 6‐, 5‐, 4‐, and 2‐carboxyl porphyrin concentrations in liver, kidney, and fecal‐urate excreta were readily detectable by high‐performance liquid chro‐matography (HPLC) spectrofluorometric techniques and displayed tissue‐specific patterns throughout the developmental period. Liver and fecal‐urate porphyrin patterns were established by d 4 subsequent to hatch and remained constant through d 17 of development, whereas renal porphyrin profiles were constant throughout the entire developmental period. In controlled field studies, nestling starlings were treated with either HgCI2or hexachlorobenzene (HCB), and tissue and excreta porphyrins were extracted and evaluated. The findings suggest that the nestling starling may serve as a suitable model species in which to monitor the effects of field contaminant exposure to wildlife based on chemical‐induced changes in tissue or excreta porphyrin levels.

ISSN:0098-4108    

DOI:10.1080/15287399309531775

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

The present studies were designed to compare the acute cytotoxic responses of cultured avian and rodent aortic smooth muscle cells (SMCs) to allylamine (AAM), a selective vascular toxin. SMCs were isolated from male Japanese quail or Sprague‐Dawley rats and established in culture fay standard procedures. Cellular glutathione (GSH) content and lactate dehydrogenase (LDH) leakage were used as indices of cytotoxicity. Exposure of avian and rodent SMCs in primary culture to AAM (0.2–200 μM) for 4 h was associated with a significant reduction in cellular CSH and enzyme leakage in cultures of both cell types. Increased exposure time to 24 h further depleted cellular CSH levels and enhanced the leakage of LDH in primary cultures of avian SMCs. In contrast, enhanced LDH leakage occurred without further CSH depletion in primary cultures of rodent SMCs upon exposure to AAM for 24 h. Removal of serum did not modulate the cytotoxic response profile of primary cultures of avian SMCs treated with 200 μM AAM, but was associated with marked elevation in cellular CSH levels and significant LDH leakage in rodent SMC cultures. The cytotoxic responses to 0.2–200 μM AAM in secondary cultures of avian SMCs were comparable to those observed in primary culture. In contrast, AAM‐induced enzyme leakage did not consistently correlate with changes in CSH content in subcul‐tured rodent SMCs. Challenge with 200 μM acrolein (ACR) for 4 h reduced the GSH content in avian, but not rodent, subcultures of SMCs. However, significant LDH leakage occurred in subcultures of both cell types upon exposure to ACR. Although hydrogen peroxide (H2O2) did not modulate GSH levels in avian or rodent cultures, leakage of LDH was observed in rat SMCs challenged with 200 μM H2O2. Removal of serum did not alter the cytotoxic responses of avian subcultures to 200 μM AAM for 24 h, but fully prevented cytotoxicity in rodent subcultures. These data suggest that potentially significant variations in the sequence of events leading to injury may exist between quail and rat aortic SMCs. These differences may contribute to the enhanced avian susceptibility to AAM‐induced aortic injury in vivo.

ISSN:0098-4108    

DOI:10.1080/15287399309531776

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

The renal disposition and the intrarenal distribution of albumin and mercury were studied simultaneously in rats co‐injected with a 0.5‐μmol/kg dose of albumin and a 0.25‐μmol/kg dose of inorganic mercury at 2, 5, 30, and 180 min after injection. These studies were carried out to test the hypothesis that one of the mechanisms involved in the renal tubular uptake of inorganic mercury is cotransport with albumin. By the end of the first 2 min after injection, the ratio of inorganic mercury to albumin in the renal cortex and outer stripe of the outer medulla was approximately 2.6 and 1.6, respectively. Both the cortex and outer stripe contain segments of the proximal tubule, and it is these segments that have been shown to be principally involved in the renal tubular uptake of both albumin and inorganic mercury. The ratio increased slightly in these two zones after 5 and 20 min after injection. These data demonstrate that there is a relatively close relationship in the renal content of inorganic mercury and albumin during the early minutes after co‐injection of inorganic mercury and albumin. However, the ratios are significantly greater than the ratio of inorganic mercury to albumin in the injection solution, which was 0.5. After 180 min following co‐injection, the ratio increased to about 38 in the cortex and 15 in the outer stripe. This increase in the ratio is probably related to the metabolism of albumin. Based on the ratios of inorganic mercury to albumin in the renal cortex and outer stripe of the outer medulla, it appears that some proximal tubular uptake of inorganic mercury occurs by mechanisms other than endocytotic cotransport of inorganic mercury with albumin. However, since the ratios were small during the early times after injection, cotransport of inorganic mercury with albumin cannot be excluded as one of the mechanisms involved in the proximal tubular uptake of inorganic mercury.

ISSN:0098-4108    

DOI:10.1080/15287399309531777

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

Technical hexachlorocyclohexane (5, 25, and 50 mg/kg/d) was orally administered to mice during the pre‐ and postimplantation period. While mice exposed to HCH during the preimplantation period did not show fetolethality, exposure during the postimplantation period showed dose‐dependent effects on fetuses as evidenced by increase in percentage resorption, higher level of HCH residue, and decreased serum progesterone level. The absence of anomalies in fetal gross morphology and skeleton suggests technical HCH is nonteratogenic in mice

ISSN:0098-4108    

DOI:10.1080/15287399309531778

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

Guinea pigs have been used extensively to model pulmonary hypersensitivity responses. Although guinea pigs produce mainly immunoglobulin G1(IgG1) antibodies and humans produce IgE, both immunoglobulin classes have been shown to be regulated similarly. We used an established guinea pig model to examine the role of IgG1in immediate‐ and late‐onset pulmonary hypersensitivity responses. IgG1was purified from the serum of ovalbumin‐immunized animals and shown to be free of IgE. It was transferred into naive recipients in doses quantified on the basis of its biological activity as measured in the passive cutaneous anaphylaxis (PCA) assay. Inhalation challenge of recipient animals 24 h later with an ovalbumin aerosol produced immediate‐onset airway constrictive responses, with response dependent upon the quantity of antibody passively administered. None of the recipient animals displayed a late‐phase response previously shown to be characterized by increased breathing frequency, airflow limitation during exhalation, and mild fever. However, pulmonary eosinophilia, measured at 24 h postinhalation challenge, was detected with the severity of the eosinophilia dependent upon the quantity of IgG, administered. The results indicated that immediate‐, but not late‐onset, responses were associated with IgG, antibody. Occurrence of late‐onset pulmonary eosinophilia indicated that eosinophilic inflammation, a recognized characteristic of hypersensitivity responses, was related to antigen‐specific IgG1antibody.

ISSN:0098-4108    

DOI:10.1080/15287399309531779

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

This study assessed effects of exposure to p‐xylene, a ubiquitous air pollutant, on mice infected with murine cytomegalovirus (MCMV), a mouse model for a common human virus. It was postulated that adverse health effects could occur as a result of (1) enhanced infection due to xylene‐induced immune suppression, (2) increased p‐xylene toxicity due to viral suppression of cytochrome P‐450 (P‐450), and/or (3) additive or synergistic effects on liver function due to tissue injury by both p‐xylene and MCMV. Mice were exposed to filtered air, 600 or 1200 ppm p‐xylene 6 h/d for 4 d and infected with a sublethal dose of MCMV after the first exposure. No deaths occurred among uninfected, p‐xylene‐exposed mice or infected, air‐exposed mice; 34% and 0% mortality occurred respectively in infected mice exposed to 1200 and 600 ppm p‐xylene. Virus titers in the liver and splenic natural killer cell activity were unaffected by exposure to 1200 ppm p‐xylene. Small but significant increases in serum aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase activities, indicators of liver damage, were observed at 4 d postin‐fection. p‐Xylene exposure had no effect on these serum enzyme activities in uninfected mice, but 1200 ppm potentiated this effect in infected mice. MCMV significantly suppressed and p‐xylene significantly increased total P‐450 levels in the liver, but there was no significant interaction between the two. Isozymes 1A1, 2B1/B2, and 2E1 were decreased to a similar degree, suggesting that the virus does not target specific isozymes. Enhanced mortality was not due to immune suppression. While p‐xylene potentiated liver damage was caused by the virus, the magnitude of serum enzyme activities indicates that this damage was not a likely cause of death. The cause of deaths is unclear, results were consistent with the hypothesis that enhanced mortality was related to enhanced xylene toxicity due to suppression of P‐450, although additive or synergistic damage to tissues other than liver cannot be ruled out.

ISSN:0098-4108    

DOI:10.1080/15287399309531780

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

ISSN:0098-4108    

DOI:10.1080/15287399309531771

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor