{"title":"Adverse health consequences of cigarette smoking also include drug interactions","authors":"L. Knodel","doi":"10.1080/107691897229829","DOIUrl":"https://doi.org/10.1080/107691897229829","url":null,"abstract":"","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90840200","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}
Bacterial systems are subjected to cellular repair of different types. A recombination (rec) repair test applied to chemicals/ carcinogens produces positive results in the rec assay. Two chromium com pounds, chromium trioxide (CrO3, MW 100.01) and potassium dichrom ate (K2Cr2O7, MW 294.21) have been subjected to rec assay. The rec effect was greater with K2Cr2O7 than with CrO3. The S9 metabolic activation mixture had a detoxifying effect for both the compounds.
{"title":"STUDIES ON THE REC EFFECTS OF CHROMIUM(VI) COMPOUNDS IN BACILLUS SUBTILIS","authors":"R. C. S. Obti, M. Kaushal, A. Kaushal","doi":"10.1080/107691897229784","DOIUrl":"https://doi.org/10.1080/107691897229784","url":null,"abstract":"Bacterial systems are subjected to cellular repair of different types. A recombination (rec) repair test applied to chemicals/ carcinogens produces positive results in the rec assay. Two chromium com pounds, chromium trioxide (CrO3, MW 100.01) and potassium dichrom ate (K2Cr2O7, MW 294.21) have been subjected to rec assay. The rec effect was greater with K2Cr2O7 than with CrO3. The S9 metabolic activation mixture had a detoxifying effect for both the compounds.","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88586380","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}
L. Friedman, D. Gaines, R. Chi, Matthew C Smith, R. Braunberg, C. Thorpe
The possible interaction between pairs of aflatoxins com monly occurring together in foods was evaluated by determining their biochem ical actions on the liver and hepatocytes of young mature rats. RNA synthesis, a sensitive and 14 early target of the effects of aflatoxin B1, was m easured with [ C]orotic acid or 3 [ H]uridine used as substrates. In the first study (comprised of four replicate experiments), liver slices treated with aflatoxin B1 at 0, 120, 240, and 480 ng/ ml were incubated in the presence and absence of aflatoxin B2 at 120 ng/ ml. In the second study, liver slices were treated with the sam e concentrations of B1 incubated in the presence and absence of aflatoxin G1 at 120 ng/ m l (comprised of four replicate experim ents) or at 240 ng/ ml (comprised of two replicate experim ents). In the third study (single experim ent), isolated hepatocytes were treated with aflatoxin B1 at 0, 60, 120, 240, and 480 ng/ ml in the presence and absence of aflatoxin G1 at 120 ng/ m l. Leakage of lactic acid...
通过测定食物中常见的黄曲霉毒素对年轻成熟大鼠肝脏和肝细胞的生化作用，评估了它们之间可能的相互作用。RNA合成是黄曲霉毒素B1作用的一个敏感的早期靶点，我们用[C]山茱萸酸或3 [H]尿苷作为底物来测定RNA合成。在第一项研究(由四个复制实验),肝片治疗黄曲霉毒素B1(0, 120, 240,和480 ng / ml孵化的存在和缺乏黄曲霉素B2 120 ng / ml。在第二项研究中,肝片治疗与山姆e浓度存在和缺乏黄曲霉毒素B1孵化的G1在120 ng / l(由四个复制experim树人)或240 ng / ml(由两个复制experim树人)。在第三项研究(单实验)中，分离的肝细胞分别用黄曲霉毒素B1 0、60、120、240和480 ng/ ml处理，黄曲霉毒素G1浓度分别为120 ng/ ml和不含黄曲霉毒素G1。
{"title":"INTERACTION OF AFLATOXINS AS MEASURED BY THEIR BIOCHEMICAL ACTION ON RAT LIVER SLICES AND HEPATOCYTES","authors":"L. Friedman, D. Gaines, R. Chi, Matthew C Smith, R. Braunberg, C. Thorpe","doi":"10.1080/107691897229775","DOIUrl":"https://doi.org/10.1080/107691897229775","url":null,"abstract":"The possible interaction between pairs of aflatoxins com monly occurring together in foods was evaluated by determining their biochem ical actions on the liver and hepatocytes of young mature rats. RNA synthesis, a sensitive and 14 early target of the effects of aflatoxin B1, was m easured with [ C]orotic acid or 3 [ H]uridine used as substrates. In the first study (comprised of four replicate experiments), liver slices treated with aflatoxin B1 at 0, 120, 240, and 480 ng/ ml were incubated in the presence and absence of aflatoxin B2 at 120 ng/ ml. In the second study, liver slices were treated with the sam e concentrations of B1 incubated in the presence and absence of aflatoxin G1 at 120 ng/ m l (comprised of four replicate experim ents) or at 240 ng/ ml (comprised of two replicate experim ents). In the third study (single experim ent), isolated hepatocytes were treated with aflatoxin B1 at 0, 60, 120, 240, and 480 ng/ ml in the presence and absence of aflatoxin G1 at 120 ng/ m l. Leakage of lactic acid...","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85682429","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}
Treatment of human leukemic T-lymphocyte MOLT4 cells with potassium chromate, a chromium (VI) compound, increased the form ation of the oxidized compound dichlorofluorescein (DCF), a highly fluorescent compound, from the parent nonfluorescent compound, 2,7-dichlorofluorescin diacetate (DCF-DA). No such increase in DCF formation was observed when cells were treated with Cr(III) compounds. In cell-free system s, dichlorofluorescin diacetate was also oxidized to DCF by strong oxidants (such as hydrogen peroxide and hydroperoxides) in the presence of peroxidase, suggesting that Cr(VI) treatment increased the intracellular level of these peroxides in MOLT4 cells. The rate of generation of peroxides was found to be both dose and time dependent. These results suggest that accumulation of intracellular peroxides may, at least in part, be associated with chromium-induced genotoxicity and add to the emerging concept that these phenomena may, in part, be mediated via oxidative m echanisms.
{"title":"CARCINOGENIC CHROMIUM(VI) INDUCES OXIDATIVE STRESS IN CULTURED HUMAN LEUKEMIC T-LYMPHOCYTES. 1. GENERATIO OF HYDROGEN PEROXIDE DURIN INTRACELLULAR REDUCTION OF CHROMATE","authors":"S. Mattagajasingh, H. Misra","doi":"10.1080/107691897229801","DOIUrl":"https://doi.org/10.1080/107691897229801","url":null,"abstract":"Treatment of human leukemic T-lymphocyte MOLT4 cells with potassium chromate, a chromium (VI) compound, increased the form ation of the oxidized compound dichlorofluorescein (DCF), a highly fluorescent compound, from the parent nonfluorescent compound, 2,7-dichlorofluorescin diacetate (DCF-DA). No such increase in DCF formation was observed when cells were treated with Cr(III) compounds. In cell-free system s, dichlorofluorescin diacetate was also oxidized to DCF by strong oxidants (such as hydrogen peroxide and hydroperoxides) in the presence of peroxidase, suggesting that Cr(VI) treatment increased the intracellular level of these peroxides in MOLT4 cells. The rate of generation of peroxides was found to be both dose and time dependent. These results suggest that accumulation of intracellular peroxides may, at least in part, be associated with chromium-induced genotoxicity and add to the emerging concept that these phenomena may, in part, be mediated via oxidative m echanisms.","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77998204","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}
Recent research on elucidation of mechanisms of the phototoxic activities of various pharmaceutical products currently being investigated in this laboratory is reviewed. Due to the importance of antibacterial quinolones of com mon use in present m edical practice, it is considered of general interest to summ arize the photochem ical reactions involved in the generation of active photoproducts and the possibility of metabolite mediation in biological damage. Thus, m echanism s are postulated for the photochemical decomposition of the substances investigated as well as the possible in vitro m echanism involved at cellular level.
{"title":"MECHANISTIC STUDIES ON PHOTOTOXICITY INDUCED BY ANTIBACTERIAL QUINOLONES","authors":"F. Vargas, C. Rivas","doi":"10.1080/107691897229810","DOIUrl":"https://doi.org/10.1080/107691897229810","url":null,"abstract":"Recent research on elucidation of mechanisms of the phototoxic activities of various pharmaceutical products currently being investigated in this laboratory is reviewed. Due to the importance of antibacterial quinolones of com mon use in present m edical practice, it is considered of general interest to summ arize the photochem ical reactions involved in the generation of active photoproducts and the possibility of metabolite mediation in biological damage. Thus, m echanism s are postulated for the photochemical decomposition of the substances investigated as well as the possible in vitro m echanism involved at cellular level.","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75915848","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}
N-Acetyl--d-glucosaminidase (NAG) is one of the sensitive hydrolytic lysosomal enzymes that is released after renal tubular damage. We have studied gentamicin-induced nephrotoxicity by determining the NAG release in a perfused rat kidney model. Gentamicin at 100 ug/ml caused a time-dependent increase in enzymuria. The effect of pretreatment with 5 or 10 mmol/kg of lithium chloride, administered subcutaneously 24 h prior to perfusion with gentamicin, was also studied through the measurement of NAG activity. Lithium at 5 mmol/kg absolutely inhibited NAG release; 10 mmol/kg lithium significantly diminished the release of enzyme. The inhibitory effect of 5 mmol/kg of lithium may be due to its interference with phosphoinositide cycle in renal tubular lysosomal membrane.
n -乙酰-d-氨基葡萄糖酶(NAG)是肾小管损伤后释放的一种敏感的水解溶酶体酶。我们通过测定灌流大鼠肾模型中NAG的释放量来研究庆大霉素引起的肾毒性。100 ug/ml庆大霉素引起酶血症的时间依赖性增加。庆大霉素灌注前24 h皮下给予5或10 mmol/kg氯化锂预处理，并通过测定NAG活性来研究预处理效果。5 mmol/kg锂绝对抑制NAG释放;10 mmol/kg锂显著降低酶的释放。5 mmol/kg锂的抑制作用可能与干扰肾小管溶酶体膜内磷酸肌苷循环有关。
{"title":"INHIBITION BY LITHIUM OF GENTAMICININDUCED RELEASE OF N-ACETYL--DGLUCOSAMINIDASE IN ISOLATED PERFUSED RAT KIDNEY","authors":"M. Djamali, M. Shahrokhi","doi":"10.1080/107691897229766","DOIUrl":"https://doi.org/10.1080/107691897229766","url":null,"abstract":"N-Acetyl--d-glucosaminidase (NAG) is one of the sensitive hydrolytic lysosomal enzymes that is released after renal tubular damage. We have studied gentamicin-induced nephrotoxicity by determining the NAG release in a perfused rat kidney model. Gentamicin at 100 ug/ml caused a time-dependent increase in enzymuria. The effect of pretreatment with 5 or 10 mmol/kg of lithium chloride, administered subcutaneously 24 h prior to perfusion with gentamicin, was also studied through the measurement of NAG activity. Lithium at 5 mmol/kg absolutely inhibited NAG release; 10 mmol/kg lithium significantly diminished the release of enzyme. The inhibitory effect of 5 mmol/kg of lithium may be due to its interference with phosphoinositide cycle in renal tubular lysosomal membrane.","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86919093","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}
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