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RELATIONSHIP BETWEEN LEAD ACCUMULATION IN BLOOD AND SOFT TISSUES OF RATS SUBCHRONICALLY EXPOSED TO LOW LEVELS OF LEAD 低铅亚慢性暴露大鼠血液中铅积累与软组织的关系
Toxic substance mechanisms Pub Date : 1999-06-01 DOI: 10.1080/107691899229115
Oluwasanmi O Areola, A. L. Jadhav, M. Williams-Johnson
{"title":"RELATIONSHIP BETWEEN LEAD ACCUMULATION IN BLOOD AND SOFT TISSUES OF RATS SUBCHRONICALLY EXPOSED TO LOW LEVELS OF LEAD","authors":"Oluwasanmi O Areola, A. L. Jadhav, M. Williams-Johnson","doi":"10.1080/107691899229115","DOIUrl":"https://doi.org/10.1080/107691899229115","url":null,"abstract":"Studies on the distribution of lead (Pb) at exposure levels that produce blood Pb levels similar to those considered a potential concern ( 10-14 mug/dl) are seriously lacking in the scientific literature. Because the manifestations of toxic effects of Pb vary depending on concentration and site of action, delineation of patterns of accumulation of Pb in tissues that may serve as sites of action at low levels of exposure may provide critical clues in elucidating the toxic effects of Pb. Also of importance is the contention that blood Pb levels may not adequately represent the potential for tissue-specific toxicity, particularly at low levels of exposure. This study was designed to examine the temporal pattern of Pb accumulation in blood and in various soft tissues during subchronic oral exposure to 5 or 50 ppm Pb. Sixty-three Long-Evans male rats (21 days old) were randomly divided into three groups and were provided 0 (50 ppm sodium acetate), 5, or 50 ppm Pb acetate in drinking water for 90 days. Rats fro...","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83101658","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}
引用次数: 8
ALTERATION BY LEAD ACETATE OF RAT SUBMANDIBULAR GLAND MORPHOLOGY AND ULTRASTRUCTURE 醋酸铅对大鼠颌下腺形态及超微结构的影响
Toxic substance mechanisms Pub Date : 1999-06-01 DOI: 10.1080/107691899229106
M. Abdollahi, M. Sharifzadeh, H. Marzban, Gholamreza Abri, Mehdi Torab-Jahromi
{"title":"ALTERATION BY LEAD ACETATE OF RAT SUBMANDIBULAR GLAND MORPHOLOGY AND ULTRASTRUCTURE","authors":"M. Abdollahi, M. Sharifzadeh, H. Marzban, Gholamreza Abri, Mehdi Torab-Jahromi","doi":"10.1080/107691899229106","DOIUrl":"https://doi.org/10.1080/107691899229106","url":null,"abstract":"Structural changes of rat submandibular glands (SMG) after long-term treatment with various doses of lead (0.01%, 0.04%, 0.05%) were investigated in this study. After termination of treatment, SMGs were removed and homogenized for measurement of total protein, DNA, calcium, and lead concentrations. Also ultrastructural examination of glands by electron microscopy was carried out. Total protein, DNA, and intracellular calcium concentrations of treated glands at 0.04% and 0.05% lead concentrations showed significant reduction when compared with those of controls. Data of lead measurement, as determined by atomic absorption spectroscopy, showed that lead treatment resulted in accumulation of lead in rats'SMGs. Lead treatment also caused degenerative changes in the cells. Dilation of rough endoplasmic reticulum (RER) and swollen mitochondria were observed in the (0.05%) treated group. Transformation and enlargement of mitochondria also were determined in the (0.04%) treated group. We propose that lead treatme...","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89401084","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}
引用次数: 10
REACTIVE ACYL GLUCURONIDES: POSSIBLE ROLE IN SMALL INTESTINAL TOXICITY INDUCED BY NONSTEROIDAL ANTI-INFLAMMATORY DRUGS 活性酰基葡萄糖醛酸酯:在非甾体抗炎药引起的小肠毒性中的可能作用
Toxic substance mechanisms Pub Date : 1999-03-01 DOI: 10.1080/107691899229160
U. Boelsterli
{"title":"REACTIVE ACYL GLUCURONIDES: POSSIBLE ROLE IN SMALL INTESTINAL TOXICITY INDUCED BY NONSTEROIDAL ANTI-INFLAMMATORY DRUGS","authors":"U. Boelsterli","doi":"10.1080/107691899229160","DOIUrl":"https://doi.org/10.1080/107691899229160","url":null,"abstract":"Small intestinal injury induced by nonsteroidal anti-inflammatory drugs (NSAIDs) has gained increasing attention in the past years. The mechanism underlying NSAID enteropathy has remained elusive but may be different from that in the stom ach. Three important factors include the presence of bile or biliary constituents, enterohepatic circulation of NSAIDs, and enteric bacteria. This article summarizes new lines of evidence indicating that acyl glucuronides, which are m etabolites of many carboxylic acid NSAIDs, m ay be causally linked with small intestinal ulceration. Acyl glucuronides are form ed in the liver; excreted into thebiliary treeby the conjugate export pump, Mrp2;and subsequently delivered to the lower intestine. Acyl glucuronides are chemically reactive and can covalently modify a number of target proteins in the liver, biliary tree, and intestine. The following article focuses on the positive correlation between the degree by which the small intestine is exposed to NSAID acyl glucuronides and...","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86549568","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}
引用次数: 7
MECHANISMS OF DECREASES IN MONOBROMOBIMANE-DERIVED FLUORESCENCE OF CARBAMYL PHOSPHATE SYNTHETASE-I FOLLOWING HEPATOTOXIC DOSES OF ACETAMINOPHEN IN MICE 小鼠肝毒性剂量对乙酰氨基酚后磷酸氨甲酰合成酶- i单溴莫西曼衍生荧光减少的机制
Toxic substance mechanisms Pub Date : 1999-03-01 DOI: 10.1080/107691899229151
Sarah K. Taylor, Charles V. Smith
{"title":"MECHANISMS OF DECREASES IN MONOBROMOBIMANE-DERIVED FLUORESCENCE OF CARBAMYL PHOSPHATE SYNTHETASE-I FOLLOWING HEPATOTOXIC DOSES OF ACETAMINOPHEN IN MICE","authors":"Sarah K. Taylor, Charles V. Smith","doi":"10.1080/107691899229151","DOIUrl":"https://doi.org/10.1080/107691899229151","url":null,"abstract":"","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85206229","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}
引用次数: 0
PHOTOTOXICITY INDUCED BY 1O2 GENERATION DURING THE PHOTODEGRADATION OF SOME DIURETIC DRUGS 某些利尿剂药物在光降解过程中产生的1o2引起的光毒性
Toxic substance mechanisms Pub Date : 1999-03-01 DOI: 10.1080/107691899229142
F. Vargas, H. Mendez, Ju
{"title":"PHOTOTOXICITY INDUCED BY 1O2 GENERATION DURING THE PHOTODEGRADATION OF SOME DIURETIC DRUGS","authors":"F. Vargas, H. Mendez, Ju","doi":"10.1080/107691899229142","DOIUrl":"https://doi.org/10.1080/107691899229142","url":null,"abstract":"","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89029941","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}
引用次数: 6
GLUTATHIONE REDOX STATUS IN THE HUMAN CELL LINE, A549, FOLLOWING INTRACELLULAR GLUTATHIONE DEPLETION AND EXTRACELLULAR GLUTATHIONE ADDITION 在细胞内谷胱甘肽消耗和细胞外谷胱甘肽添加后，人类细胞系中的谷胱甘肽氧化还原状态，a549
Toxic substance mechanisms Pub Date : 1999-01-01 DOI: 10.1080/107691899229205
J. A. Pendergrass, Jr. V. Srinivasan E. P. Clark K. S. Kumar
{"title":"GLUTATHIONE REDOX STATUS IN THE HUMAN CELL LINE, A549, FOLLOWING INTRACELLULAR GLUTATHIONE DEPLETION AND EXTRACELLULAR GLUTATHIONE ADDITION","authors":"J. A. Pendergrass, Jr. V. Srinivasan E. P. Clark K. S. Kumar","doi":"10.1080/107691899229205","DOIUrl":"https://doi.org/10.1080/107691899229205","url":null,"abstract":"The redox status of glutathione (L-gamma-glutamyl-L-cysteinylglycine, GSH) plays an im portant role in a number of different cellular reactions including cellular oxidative stress. Using A549 human...","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86984335","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}
引用次数: 2
EFFECTS OF LEAD ACETATE EXPOSURE ON NALOXONE-INDUCED JUMPING BEHAVIOR IN MICE 醋酸铅暴露对纳洛酮诱导小鼠跳跃行为的影响
Toxic substance mechanisms Pub Date : 1999-01-01 DOI: 10.1080/107691899229223
Mahmoud Ghazi-Khansari Bahram Delfa
{"title":"EFFECTS OF LEAD ACETATE EXPOSURE ON NALOXONE-INDUCED JUMPING BEHAVIOR IN MICE","authors":"Mahmoud Ghazi-Khansari Bahram Delfa","doi":"10.1080/107691899229223","DOIUrl":"https://doi.org/10.1080/107691899229223","url":null,"abstract":"","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77680761","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}
引用次数: 4
LEUKOCYTE HYPOCELLULARITY IN THE SPLEEN AND PRONEPHROS OF TILAPIA (OREOCHROMIS NILOTICUS) EXPOSED TO 2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN (TCDD) MAY RESULT FROM ANTIPROLIFERATIVE EFFECTS AND ENHANCED APOPTOSIS 摘要罗非鱼(OREOCHROMIS NILOTICUS)暴露于2,3,7,8-四氯二苯并-对二恶英(TCDD)后，脾脏和肾原的白细胞减少可能是由抗增殖作用和细胞凋亡增强引起的
Toxic substance mechanisms Pub Date : 1999-01-01 DOI: 10.1080/107691899229214
L. Gogal
{"title":"LEUKOCYTE HYPOCELLULARITY IN THE SPLEEN AND PRONEPHROS OF TILAPIA (OREOCHROMIS NILOTICUS) EXPOSED TO 2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN (TCDD) MAY RESULT FROM ANTIPROLIFERATIVE EFFECTS AND ENHANCED APOPTOSIS","authors":"L. Gogal","doi":"10.1080/107691899229214","DOIUrl":"https://doi.org/10.1080/107691899229214","url":null,"abstract":"Tilapia (Oreochromis niloticus) were subacutely exposed to the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) by intraperitoneal injection of 1 or 5 mug/kg/day for five consecutive days. Cellularity and morphology of the spleen and pronephros were evaluated two days following dosing. Total cell counts in both the spleen and pronephros were significantly reduced by the 5-mug/kg but not the 1-mug/kg dose of TCDD. Cellular depletion was evident histologically at the higher dose level, particularly within lymphoid regions of the fish spleen and pronephros. Increased numbers of apoptotic cells were observed in the histologic preparations. Light microscopic analysis of cytospin samples from the pronephros of chemical-treated fish verified the increased incidence of cells displaying features typical of apoptosis (condensed nuclei and cytoplasmic fragmentation). Subsequent flow cytom etric evaluation using the DNA-binding dye, 7-aminoactinomycin D (7-AAD), demonstrated a population of apopto...","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88640081","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}
引用次数: 7
PHENOBARBITAL ALTERS LIVER AND KIDNEY FUNCTION IN TOLUENE- AND TRICHLOROETHYLENE-TREATED RATS 苯巴比妥可改变甲苯和三氯乙烯处理大鼠的肝肾功能
Toxic substance mechanisms Pub Date : 1999-01-01 DOI: 10.1080/107691899229197
S. Gupta
{"title":"PHENOBARBITAL ALTERS LIVER AND KIDNEY FUNCTION IN TOLUENE- AND TRICHLOROETHYLENE-TREATED RATS","authors":"S. Gupta","doi":"10.1080/107691899229197","DOIUrl":"https://doi.org/10.1080/107691899229197","url":null,"abstract":"Effects of two widely used industrial solvents-toluene and trichloroethyleneon liver and kidney function have been studied in laboratory rats after microsomal induction with phenobarbital. Higher efflux of GOT and GPT suggests that phenobarbital pretreatment stimulates hepatic toxicity of toluene in rats. However, a decline in GPT was recorded in phenobarbital- and trichloroethylenetreated rats. Further, observations on alkaline phosphatase suggest that the metabolic disposition of toluene and trichloroethylene is altered by pretreatment with phenobarbital. Phenobarbital potentiates the necrotizing damage caused by toluene; however, it offers protection against cholestatic injury. In trichloroethylene-treated rats as well, only partial protection could be offered by phenobarbital. Pretreatment of rats with phenobarbital results in a noticeable stim ulation of hepatic cytochrome P450s that are responsible for the metabolism of various drugs and xenobiotics. However, responses are typified by the multiple f...","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74176832","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}
引用次数: 6
Modification of the adverse effects of cadmium exposure by steroid compounds in rodents: A review 类固醇化合物对啮齿动物镉暴露不良反应的影响:综述
Toxic substance mechanisms Pub Date : 1998-11-04 DOI: 10.1080/107691898229260
H. Shimada, M. Takiguchi, M. Waalkes
{"title":"Modification of the adverse effects of cadmium exposure by steroid compounds in rodents: A review","authors":"H. Shimada, M. Takiguchi, M. Waalkes","doi":"10.1080/107691898229260","DOIUrl":"https://doi.org/10.1080/107691898229260","url":null,"abstract":"Cadmium is a very important m etal toxin and environmental pollutant. In rodents, the acute and chronic toxic effects of cadmium are pronounced in several tissues including the lung, liver, kidney, prostate, and testes. The toxic effects of cadmium can be modulated by pretreatments or concurrent treatments with various m etallic and nonmetallic substances. This review focuses on theeffects of steroid hormones and steroid antagonists on cadmium toxicity in vivo. Steroids can have a variety of effects on cadmium toxicity including both mitigation and exacerbation of the adverse effects of this metal. Steroids or steroid antagonists that have been reported to modify cadmium toxicity include testosterone, progesterone, cyproterone, estradiol, and stilbestrol. Some steroids, like dexam ethasone and corticosterone, are inducers of metallothionein (MT), a cadmium-binding protein thought to be im portant in cadm ium tolerance. From these reports several possible mechanisms have been proposed to explain the m odul...","PeriodicalId":87425,"journal":{"name":"Toxic substance mechanisms","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1998-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85260336","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}
引用次数: 3
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