Journal of toxicology and environmental health最新文献

{"title":"Activity of esterases from different tissues of freshwater fish and responses of their isoenzymes to inhibitors.","authors":"S N Li,&nbsp;D F Fan","doi":"10.1080/00984109708984018","DOIUrl":"https://doi.org/10.1080/00984109708984018","url":null,"abstract":"<p><p>Activity of nonspecific esterase from different tissues (i.e., liver, gallbladder, heart, intestine, and muscle) of five species of freshwater fish, namely, topmouth gudgeon (Pseudorasbora parva), goldfish (Carassius auratus), nile tilapia (Tilapia nilotica), mosquitofish (Gambusia affinis), and rainbow trout (Salmo gairdneri) was tested using alpha-naphthyl acetate as substrate. The results indicated that activity of the enzyme was mainly concentrated in the digestive system (i.e., intestine, liver, bile). The overall activity was highest in nile tilapia, followed by mosquitofish, topmouth gudgeon, goldfish, and lowest in rainbow trout. Electrophoresis and the following in vitro treatment of the isoenzymes with triphenol phosphate (TPP, an inhibitor of carboxylesterase) indicated the TPP-sensitive esterase was mainly distributed in liver of the five species. The enzyme was not found in the other five tissues (including gill) except in gallbladder of topmouth gudgeon and goldfish. The correlation was obviously improved between susceptibility and detoxification capacity if activity of the TPP-sensitive esterase was employed instead of that of the nonspecific esterase to make the comparison. In vitro treatment of nonspecific esterase in liver with malaoxon proved that the active metabolite of malathion inhibited a different isoenzyme from the TPP-sensitive one.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 2","pages":"149-57"},"PeriodicalIF":0.0,"publicationDate":"1997-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20123591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of mouse strains for susceptibility to styrene-induced hepatotoxicity and pneumotoxicity.","authors":"G P Carlson","doi":"10.1080/00984109708984020","DOIUrl":"https://doi.org/10.1080/00984109708984020","url":null,"abstract":"<p><p>Styrene is known to cause both hepatotoxicity and pneumotoxicity in mice. Strain differences have been reported by other investigators suggesting that Swiss mice are less susceptible than non-Swiss mice to styrene-induced liver damage. In this study, A/J and C57BL/6 mice were found to be similar to non-Swiss albino (NSA) mice in susceptibility whereas CD-1 (Swiss) mice were more resistant to hepatotoxicity as assessed by serum sorbitol dehydrogenase levels and pneumotoxicity as determined by gamma-glutamyltranspeptidase and lactate dehydrogenase measurements in bronchoalveolar lavage fluid. Styrene was hepatotoxic in CD-1 mice treated with pyridine to induce CYP2E1. CYP2E1 apoprotein levels and p-nitrophenol hydroxylase activities in control and pyridine-induced mice were similar in the two strains. Hepatic and pulmonary microsomal preparations from both strains metabolized styrene to styrene oxide at similar rates. CD-1 mice were as susceptible as the NSA mice to the effects of styrene oxide. The data suggest that there are no differences in the bioactivation of styrene to styrene oxide or innate susceptibility to the active metabolite that would account for the differences between the CD-1 and NSA mice.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 2","pages":"177-87"},"PeriodicalIF":0.0,"publicationDate":"1997-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20123593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mercury content in skin-lightening creams and potential hazards to the health of Saudi Women.","authors":"I al-Saleh,&nbsp;I al-Doush","doi":"10.1080/00984109708984016","DOIUrl":"https://doi.org/10.1080/00984109708984016","url":null,"abstract":"<p><p>It seems evident from a wealth of scientific research that mercury is toxic. Because of the nature of the Saudi markets, different brands of skin-lightening creams are widely available. In this study, 38 skin-lightening cream samples were collected and analyzed for mercury by inductively coupled plasma spectrometry after an acid digestion procedure. About 45% of the tested skin-lightening cream samples contained mercury at levels well above the FDA's acceptable limit of 1 ppm. These findings are alarming and have wide legal and educational implications for Saudi Arabia in particular and developing countries in general. Further investigation for possible adverse health effects is also needed.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 2","pages":"123-30"},"PeriodicalIF":0.0,"publicationDate":"1997-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20122522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tributyltin potentiates 3,3',4,4',5-pentachlorobiphenyl-induced cytochrome P-4501A-related activity.","authors":"G T DeLong,&nbsp;C D Rice","doi":"10.1080/00984109708984017","DOIUrl":"https://doi.org/10.1080/00984109708984017","url":null,"abstract":"<p><p>Induction of cytochrome P-4501A protein and induction of related enzyme activity are hallmark physiological responses following exposure to planar halogenated aromatic hydrocarbons (HAHs) such as 3,3',4,4',5-pentachlorobiphenyl (PCB 126; PeCB). Environments contaminated by HAHs are often contaminated by mixtures of anthropogenic contaminants, including organometallic compounds. Both HAHs and organometallics easily bioconcentrate and bioaccumulate in aquatic food chains that may ultimately be linked to humans through seafood consumption. Tributyltin (TBT), a marine biocide, has been detected in many aquatic environments due to its primary use as a marine antifoulant agent. Exposure to TBT, as well as several PCBs, has been associated with immunotoxicity, neurotoxicity, and endocrine disruption. Recently TBT has been shown to inhibit cytochrome P-4501A activity in vitro, but information concerning these effects in vivo and in combination with classical inducers of P-4501A, such PeCB, is lacking. We exposed female B6C3F1 mice to 0.01, 0.1, and 1.0 mg/kg PeCB, TBT, or both in combination, with corn oil (CO) serving as a carrier control. Cytochrome P-4501A protein levels and related benzo[a]pyrene hydroxylation (BaP-OHase) activity were measured following a single acute intraperitoneal (ip) dose or seven daily injections. Body, thymus, and liver weights were used to monitor general physiological responses following exposure. P-4501A levels and BaP-OHase activity were significantly elevated in mice exposed to PeCB alone. This effect was enhanced by coexposure to low levels of TBT; PeCB-induced P-4501A-related activity was potentiated at the low range of each. The highest dose of TBT, however, inhibited these activities when given in combination with PeCB. Thymic atrophy was evident only in mice exposed daily to 0:1 and 1.0 mg/kg PeCB alone, or to a combination of the lowest and highest dose of PeCB and TBT, respectively. Because environmental levels of TBT are not expected to be as high as the highest level used in our toxicological studies, we conclude that environmental exposure to TBT may potentiate, rather than inhibit, the activity of environmental levels of HAHs that are associated with P-4501A induction.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 2","pages":"131-48"},"PeriodicalIF":0.0,"publicationDate":"1997-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20122523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduction of the ex vivo production of tumor necrosis factor alpha by alveolar phagocytes after administration of coal fly ash and copper smelter dust.","authors":"F Broeckaert,&nbsp;J P Buchet,&nbsp;F Huaux,&nbsp;C Lardot,&nbsp;D Lison,&nbsp;J W Yager","doi":"10.1080/00984109708984021","DOIUrl":"https://doi.org/10.1080/00984109708984021","url":null,"abstract":"<p><p>We investigated the effect of intratracheally instilled coal fly ash (FA) and copper smelter dust (CU) on the lung integrity and on the ex vivo release of tumor necrosis factor alpha (TNF-alpha) by alveolar phagocytes. Groups of female NMRI mice received a single intratracheal administration of different particles normalized for the arsenic content (20 micrograms/kg body weight, i.e., 600 ng arsenic/mouse) and the particle load (100 mg/kg body weight, i.e., 3 mg/mouse). Mice received tungsten carbide (WC) alone (100 mg/kg), FA alone (100 mg/kg, i.e., 20 micrograms arsenic/kg), CU mixed with WC (CU, 13.6 mg/kg, i.e., 20 micrograms arsenic/kg; WC, 86.4 mg/kg) and Ca3(AsO4)2 mixed with WC (20 micrograms arsenic/kg; WC, 100 mg/kg). Animals were sacrificed at 1, 6, or 30 d posttreatment and analyzed by bronchoalveolar lavage for total protein (TP) content, inflammatory cell number and type, and TNF-alpha production. Additional mice were studied to evaluate particle retention by measuring total arsenic retention in the lung at appropriate times. Instillation of WC induced a mild and transient (d 1) inflammatory reaction characterized by an increase of TP and an influx of polymorphonuclear leukocytes in the alveolar compartment. Compared to WC, Ca3(AsO4)2 produced a significant increase of TP content in BALF. CU particles caused a severe but transient inflammatory reaction, while a persisting alveolitis (30 d) was observed after treatment with FA. Compared to control saline, a marked inhibition of TNF-alpha release was observed in response to LPS in all groups at d 1. Cytokine production was upregulated in WC- and Ca3(AsO4)1-treated animals after 6 and 30 d, respectively. However, a 90% inhibition of TNF-alpha production was still observed at d 30 after administration of CU and FA. Although arsenic was cleared from the lung tissue 6 d after Ca3(AsO4)2 administration, a significant fraction persisted (10-15% of the arsenic administered) in the lung of CU- and FA-treated mice at d 30. We hypothetize that suppression of TNF-alpha production is dependent upon the slow elimination of the particles and their metal content from the lung.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 2","pages":"189-202"},"PeriodicalIF":0.0,"publicationDate":"1997-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20123594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Attitudes toward environmental hazards: where do toxic wastes fit?","authors":"J Burger,&nbsp;M Martin,&nbsp;K Cooper,&nbsp;M Gochfeld","doi":"10.1080/00984109708984015","DOIUrl":"https://doi.org/10.1080/00984109708984015","url":null,"abstract":"<p><p>The public is continually faced with making decisions about the risks associated with environmental hazards, and, along with managers and government officials, must make informed decisions concerning possible regulation, mitigation, and restoration of degraded sites or other environmental threats. We explored the attitudes regarding several environmental hazards of six groups of people: undergraduate science majors, undergraduate nonscience majors, and graduate students in environmental health, in ecological risk assessment, and in nonscience disciplines, as well as nonstudents over 35 yr of age. We had predicted that there would be significant differences in attitudes between science and nonscience majors and as a function of age. Relative concerns could be divided into three discrete classes (in descending order of concern): (1) general ecological problems (cutting tropical forests, polluting groundwater, trash along the coasts, lead in drinking water, and acid rain), (2) radon and nuclear wastes, and finally (3) specific nuclear waste facilities, chromium, fertilizers and pesticides, and electromagnetic waves. For any hazard, attitudes were consistent across groups with regard to ranking the severity of the environmental problem and willingness to expend funds to solve the problems. Attitudes about spending money to develop methods to evaluate risk fell in the middle level of concern. There were no major differences among classes of college-age students, or between them and older nonstudents.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 2","pages":"109-21"},"PeriodicalIF":0.0,"publicationDate":"1997-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20122521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polycyclic aromatic hydrocarbon-DNA adducts in beluga whales from the Arctic.","authors":"A Mathieu,&nbsp;J F Payne,&nbsp;L L Fancey,&nbsp;R M Santella,&nbsp;T L Young","doi":"10.1080/00984109708984006","DOIUrl":"https://doi.org/10.1080/00984109708984006","url":null,"abstract":"<p><p>The Arctic is still relatively pristine in nature, but it is also vulnerable to pollution because contaminants originating from midlatitudes are transported to the Arctic by atmospheric processes, ocean currents, and rivers (Muir et al., 1992). Recognition of this fact of Arctic vulnerability has resulted in a Declaration on the Protection of the Arctic Environment by eight Arctic countries. A manifest aim of this declaration is to develop an Arctic Monitoring and Assessment Program. We report here on the presence of measurable levels of polycyclic aromatic hydrocarbon-DNA adducts, including relatively high levels in Arctic beluga (Delphinapterus leucas). These results lend support to the value of developing biological assessment programs for Arctic wildlife.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"1997-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20114918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interaction of ozone exposure with airway hyperresponsiveness and inflammation induced by trimellitic anhydride in sensitized guinea pigs.","authors":"J Sun,&nbsp;K F Chung","doi":"10.1080/00984109708984012","DOIUrl":"https://doi.org/10.1080/00984109708984012","url":null,"abstract":"<p><p>The effect of prior ozone (O3) exposure on airway hyperresponsiveness and inflammation induced by trimellitic anhydride (TMA) has been investigated in TMA-sensitized guinea pigs. Airway responsiveness was measured as the concentration of acetylcholine needed to increase baseline lung resistance (RL) by 300% (PC300). Ozone (3 ppm for 3 h) caused an increase in -log PC300 at 1 h after exposure, with return of -log PC300 to control levels at 8 h. Ozone also increased baseline RL at 8 h. TMA challenge increase -log PC300 in TMA-sensitized guinea pigs at 8 h after challenge from 3.85 +/- 0.09 to 4.11 +/- 0.09. Ozone exposure prior to TMA challenge prevented the induction of airway hyperresponsiveness with a mean -log PC300 of 3.51 +/- 0.20, which was not different from that of control TMA-sensitized group. Baseline RL was significantly higher in ozone-pretreated animals after TMA challenge when compared to those of either control or challenged with TMA alone. Ozone had no effect on TMA challenge-induced BAL eosinophilia and neutrophilia. We conclude that a single exposure to ozone inhibits the increase in airway responsiveness but increases the bronchoconstrictor response induced by TMA in TMA-sensitized guinea pigs; however, the inflammatory airway response to TMA is unchanged by preexposure to ozone.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 1","pages":"77-87"},"PeriodicalIF":0.0,"publicationDate":"1997-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20114835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elimination of beta-hexachlorocyclohexane in occupationally exposed persons.","authors":"D Jung,&nbsp;H Becher,&nbsp;L Edler,&nbsp;D Flesch-Janys,&nbsp;P Gurn,&nbsp;J Konietzko,&nbsp;A Manz,&nbsp;O Päpke","doi":"10.1080/00984109708984009","DOIUrl":"https://doi.org/10.1080/00984109708984009","url":null,"abstract":"<p><p>The elimination of beta-hexachlorocyclohexane (beta-HCH) in humans was investigated in a group of 40 former workers of a lindane-producing plant by analyzing at least 2 blood specimens (3 specimens in 3 workers) from different time points. Assuming a first-order kinetic model for excretion, the median half-life of beta-HCH is 7.2 yr calculated by concentrations in whole blood and 7.6 yr calculated by concentrations in extractable lipids. In univariate analyses an influence of age, percent body fat, and liver disease (additionally in whole blood an influence of contents of extractable lipids) on clearance was observed. All factors show a positive correlation with half-life. According to a multiple regression model, influence of percent body fat calculated according to Deurenberg et al. (1991) is an important covariate in the description of the variations of the clearance rate (calculated on the basis of extractable lipids) of beta-HCH. The data support the assumption of first-order kinetics.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 1","pages":"23-34"},"PeriodicalIF":0.0,"publicationDate":"1997-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20114921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simulated dermal contamination with capillary samples and field cholinesterase biomonitoring.","authors":"K L Yuknavage,&nbsp;R A Fenske,&nbsp;D A Kalman,&nbsp;M C Keifer,&nbsp;C E Furlong","doi":"10.1080/00984109708984010","DOIUrl":"https://doi.org/10.1080/00984109708984010","url":null,"abstract":"<p><p>The extensive international use of organophosphorus compounds (OP) results in numerous acute intoxications each year. OPs inhibit acetylcholinesterase, the enzyme responsible for breaking down the neurotransmitter acetylcholine. The World Health Organization recognizes cholinesterase (ChE) biomonitoring as a preventive measure against OP overexposure. The aim of this study was to determine if dermal OP contamination could interfere with current field ChE biomonitoring assays, which use a fingerstick blood sample. In this study we also sought to determine if high levels of a plasma enzyme, A-esterase, could protect ChE from inhibition by hydrolyzing environmentally generated oxons potentially present in a fingerstick sample. A heparinized venous blood sample was collected from a volunteer. Erythrocyte acetylcholinesterase (AChE) and plasma butyrylcholinesterase (PChE) activities were measured using a field-based colorimetric cholinesterase kit. ChE dose-response curves were constructed by allowing 10-microliters blood samples to contact environmentally realistic levels of OP thioate and oxon for 10 s. An inhibition threshold could not be established for PChE when exposed to oxon within the time necessary to perform a fingerstick analysis. AChE was also inhibited by trace amounts of oxon consistent with previously reported environmental levels. These findings suggest that the reliability of field-based biomonitoring results is limited if OP residues remain on a skin surface at the time of sample collection. A-esterase's role in protecting ChE activity was investigated using capillary and venous blood from 30 unexposed individuals. Baseline ChE activities were measured, as were individual A-esterase activities using paraoxon, diazoxon, and phenylacetate as substrates. Results were then compared to ChE activities measured after 10 s of contact with an environmentally realistic amount of OP, containing 1% oxon. Both ChE activities were significantly inhibited, with capillary values being significantly more inhibited than their venous counterparts. However, no protective effect could be associated between the degree of A-esterase activity and the subsequent level of ChE inhibition observed in an individual's blood. These results suggest that (1) if there is any uncertainty about OP skin contamination, venous blood would be a more appropriate specimen to employ when using field ChE biomonitoring kits--it is collected in larger volumes and has essentially no direct contact to dermal surfaces; and (2) A-esterase activity demonstrates no protective effect against ChE inhibition upon a blood droplet's brief contact with an OP residue containing traces of oxon.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 1","pages":"35-55"},"PeriodicalIF":0.0,"publicationDate":"1997-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20114922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}