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1. |
EFFECTS OF MOTORCYCLE EXHAUST ON CYTOCHROME P-450-DEPENDENT MONOOXYGENASES AND GLUTATHIONE S-TRANSFERASE IN RAT TISSUES |
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Journal of Toxicology and Environmental Health, Part A,
Volume 54,
Issue 7,
1998,
Page 509-527
Tzuu-Huei Ueng Wen-Po Hwang Ruei-Ming Chen Hui-Wu Wang Min-Liang Kuo Sang S. Park F. Peter Guengerich,
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摘要:
The effects of motorcycle exhaust (ME) on cytochrome P-450 (P-450) -dependent monooxygenases were determined using rats exposed to the exhaust by either inhalation, intratracheal, or intraperitoneal administration. A 4-wk ME inhalation significantly increased benzo[a]pyrene hydroxylation, 7-ethoxyresorufin O-deethylation, and NADPH-cytochrome c reductase activities in liver, kidney, and lung microsomes. Intratracheal instillation of organic extracts of ME particulate (MEP) caused a dose- and time-dependent significant increase of monooxygenase activity. Intratracheal treatment with 0.1 g MEP extract/ kg markedly elevated benzo[a]pyrene hydroxylation and 7- ethoxyresorufin O-deethylation activities in the rat tissues 24 h following treatment. Intraperitoneal treatment with 0.5 g MEP extract/ kg/d for 4d resulted in significant increases of P-450 and cytochrome b contents and NADPH-cytochrome c reductase 5 activity in liver microsomes. The intraperitoneal treatment also markedly increased monooxygenases activities toward methoxyresorufin, aniline, benzphetamine, and erythromycin in liver and benzo[a]pyrene and 7-ethoxyresorufin in liver, kidney, and lung. Immunoblotting analyses of microsomal proteins using a mouse monoclonal antibody (Mab) 1-12-3 against rat P-450 1A1 revealed that ME inhalation, MEP intratracheal, or MEP intraperitoneal treatment increased a P-450 1A protein in the hepatic and extrahepatic tissues. Protein blots analyzed using antibodies to P-450 enzymes showed that MEP intraperitoneal treatment caused increases of P-450 2B, 2E, and 3A subfamily proteins in the liver. The ME inhalation, MEP intratracheal, or MEP intraperitoneal treatment resulted in significant increases in glutathione S -transferase activity in liver cytosols. The present study shows that ME and MEP extract contain substances that can induce multiple forms of P-450 and glutathione S-transferase activity in the rat.
ISSN:1528-7394
DOI:10.1080/009841098158674
出版商:Informa UK Ltd
年代:1998
数据来源: Taylor
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2. |
ANALYSIS OF AIR POLLUTION PARTICULATE-MEDIATED OXIDANT STRESS IN ALVEOLAR MACROPHAGES |
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Journal of Toxicology and Environmental Health, Part A,
Volume 54,
Issue 7,
1998,
Page 529-545
Carroll-Ann W. Goldsmith Amy Imrich, Hadi Danaee YaoYu Ning,
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摘要:
Adverse health effects of urban air pollution particulates may be attributable to particle mediated oxidant stress and inflammation. Intracellular oxidant production in normal hamster alveolar macrophages (AMs) was measured upon exposure to concentrated ambient particulates (CAPs), residual oil fly ash (ROFA), and their water-soluble and particulate fractions. ROFA and CAPs caused increases in dichlorofluorescin (DCFH) oxidation, a fluorescent measure of intracellular reactive oxygen species (ROS) production, comparable to the positive control, phorbol myristate acetate (PMA). The water-soluble component of both CAPs and ROFA (CAPs, S and ROFA, S) significantly increased AM oxidant production over negative control. CAPs samples and components showed substantial day-to-day variability in their oxidant effects. Metal chelation by desferrioxamine (DF, 1 mM) caused significant inhibition of particulate-induced AM oxidant production. ROFA exposure resulted in increased macrophage inflammatory protein-2 (MIP-2) message in AMs and in increased tumor necrosis factor alpha(TNF-alpha) production by the monocyte-macrophage cell line, RAW 264.7. TNF- production was inhibitable by the antioxidant N -acetylcysteine (NAC). The data suggest that metal components adsorbed to urban air pollution particulates can significantly contribute to particulate ability to cause oxidant stress and cytokine production in AMs.
ISSN:1528-7394
DOI:10.1080/009841098158683
出版商:Informa UK Ltd
年代:1998
数据来源: Taylor
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3. |
ACUTE EXPOSURE TO MERCURY FROM AMALGAM: NO SHORT-TIME EFFECT ON THE PERIPHERAL BLOOD LYMPHOCYTES IN HEALTHY INDIVIDUALS |
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Journal of Toxicology and Environmental Health, Part A,
Volume 54,
Issue 7,
1998,
Page 547-560
Annika Loftenius Gunilla Sandborgh-Englund Jan Ekstrand,
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摘要:
Mercury, released from dental amalgam, has been considered to adversely affect the human immune system. This study has been performed in order to evaluate if an acute low-dose mercury exposure, achieved by total amalgam removal in 10 healthy individuals, would affect the immunocompetent cells in human blood when the mercury level in blood and plasma was increasing. Induction of lymphocyte proliferation, measured as spontaneous de novo DNA synthesis, and total T cells, CD4+ T cells, CD8+ T cells, and B cells, was studied prior to and 7, 31, and 48 h after amalgam removal. In addition, the levels of interleukin-6 (IL-6) and C-reactive protein (CRP) in serum/ plasma were measured. Despite a significant increase of the plasma mercury levels within 24 h after intervention, no significant influence on the peripheral blood lymphocytes could be detected during the first 48 h. The serum IL-6 levels increased significantly within 48 h after intervention, but were still low and within normal range. No influence on the CRP levels up to 7 d after amalgam removal was detected.
ISSN:1528-7394
DOI:10.1080/009841098158692
出版商:Informa UK Ltd
年代:1998
数据来源: Taylor
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4. |
LACK OF SUPPRESSIVE EFFECTS OF MIXTURES CONTAINING LOW LEVELS OF METHYLMERCURY (MeHg), POLYCHLORINATED DIBENZO-p-DIOXINS (PCDDS), POLYCHLORINATED DIBENZOFURANS (PCDFS), AND AROCLOR BIPHENYLS (PCBS) ON MIXED LYMPHOCYTE REACTION, PHAGOCYTIC, AND NATURAL KILLER CELL ACTIVITIES OF RAT LEUKOCYTES IN VITRO |
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Journal of Toxicology and Environmental Health, Part A,
Volume 54,
Issue 7,
1998,
Page 561-577
Felix O. Omara Denis Flipo Charles Brochu Francine Denizeau Edouard F. Potworowski Michel Fournier,
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摘要:
Rat splenocyte mixed leukocyte reaction (MLR), splenic natural killer (NK) cell activity, and phagocytic activities of splenic, peritoneal, and peripheral blood leukocytes (PBLs) were evaluated in vitro to determine the immunotoxicity of mixtures containing low levels of methylmercury (MeHg) , polychlorinated dibenzo-p-dioxins (PCDDs) , polychlorinated dibenzofurans (PCDFs), and Aroclor polychlorinated biphenyls (PCBs). The mixtures were based on the concentrations of the chemicals in fish flesh. Leukocytes from male Fischer rats were exposed to MeHg (0.1-2 mug/ml), PCDD/ PCDF mixtures (1-15 pg/ ml) of three PCDDs (2,3,7,8-tetrachlorodibenzo- p -dioxin, 1,2,3,7,8-pentachlorodibenzo-p-dioxin, and 1,2,3,4,7,8-hexachlorodibenzo-p-dioxin) and two PCDFs (2,3,7,8-tetrachlorodibenzofuran and 1,2,3,7,8-pentachlorodibenzofuran), three Aroclor PCB (Aroclor 1242, 1254, and 1260) mixtures (0.01-0.5 mug/ml), or combinations of MeHg/ PCB/ PCDD/ PCDF mixtures for 24 or 72 h before immunological assays. Phagocytosis and NK cell cytotoxicity were evaluated with a flow cytometer, and MLR of Fischer rat responder splenocytes cultured with mitomycin C-treated Long-Evans splenocytes by [3H]thymidine uptake. Exposure to MeHg (2 mug/ml) alone or with PCB/ PCDD/PCDF resulted in significant cytolethality in rat splenocytes, peritoneal leukocytes, and PBLs at 24 h exposure. Treatment with Aroclor PCB mixtures, PCDD/PCDF mixtures, 0.1 mug MeHg/ml (noncytolethal), or PCB/PCDD/ PCDF mixtures with 0.1 mug MeHg/ml caused no suppression of splenocyte MLR response, splenic NK cell-mediated lysis of Yac-1 cells, or phagocytosis of fluorescent beads by splenic, peritoneal, and peripheral blood phagocytic cells. The results indicate that in vitro exposure of rat leukocytes to low levels of MeHg, Aroclor PCB mixtures, PCDD/ PCDF mixtures, or MeHg/PCB/PCDD/PCDF mixtures had no suppressive effects on the immune functions assayed, and thus produced no additive immunotoxicity. However, in order to predict the potential risk of these chemical mixtures to the human immune system, in vivo animal studies with blood (tissue) levels compatible with the levels of MeHg, PCBs, and PCDDs/PCDFs in exposed human populations should be evaluated.
ISSN:1528-7394
DOI:10.1080/009841098158700
出版商:Informa UK Ltd
年代:1998
数据来源: Taylor
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5. |
ENVIRONMENTAL CAUSES FOR SINONASAL CANCERS IN PET DOGS, AND THEIR USEFULNESS AS SENTINELS OF INDOOR CANCER RISK |
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Journal of Toxicology and Environmental Health, Part A,
Volume 54,
Issue 7,
1998,
Page 579-591
John A. Bukowski Daniel Wartenberg Michael Goldschmidt,
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摘要:
A case-control study was conducted to investigate the environmental causes of sinonasal cancers among pet dogs. Sinonasal cancer (SNC) cases and digestive cancer controls from the years 1989 through 1993 were obtained from a veterinary histopathology database. Owners were mailed a self-administered survey requesting information on canine factors, owner demographics, household exposures (including environmental tobacco smoke), and local pollution. A total of 129 case owners and 176 control owners returned completed surveys: a response rate of approximately 72% . Only household exposures were associated with increased SNC risk. Use of indoor coal or kerosene heaters represented the strongest risk factors, with significant adjusted odds ratios of 4.2 and 2.2 respectively. Environmental tobacco smoke exposure was not a risk factor and was suggestive of a nonsignificant, mildly protective effect at the lower exposure levels. Increasing nasal length was a significant risk factor, and there was effect modification between nasal length and coal or kerosene combustion. No self-reported measures of local pollution, such as urban status or residence within 1 mile of a factory, were associated with SNC risk. These results suggest that canine SNC has a strong environmental component and highlight the importance of indoor exposures, especially from fossil fuel combustion products. These results also suggest that pet dogs represent excellent sentinels for indoor cancer risk and that canine SNC cases can be used as early markers of household exposure to carcinogenic combustion products.
ISSN:1528-7394
DOI:10.1080/009841098158719
出版商:Informa UK Ltd
年代:1998
数据来源: Taylor
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