Pub Date : 1983-02-01DOI: 10.1080/15287398309530342
K. S. Khera, C. Whalen, F. Iverson
Teratogenicity of ethylenethiourea (ETU) was studied in the hamster to define the organ most vulnerable to its teratogenic action. A single intragastric dose of 600, 1200, 1800 or 2400 mg ETU/kg was given in 1.5% aqueous gelatin on d 11 of pregnancy. None of these dose levels produced any apparent maternal toxicity. However, fetal toxicity was apparent in the form of deaths, reduced body weight at the 2400 mg/kg dose, and dose‐related incidences of hydrocephalus, hypoplastic cerebellum, cleft palate, delayed calvarial ossification, and ectrodactyly. The ventricular system of the brain and the cerebellum were among the most sensitive sites for malformations. Effects of metabolic modifiers on the teratogenicity of ETU were studied in separate experiments. Doses of ETU were administered by gastric intubation on d 11 of pregnancy either immediately after an intragastric dose of 200 or 400 mg N‐methyl‐2‐thioimidazole/kg, or 1 h after an ip 40‐mg/kg dose of SKF‐525A. The SKF‐525A pretreatment significantly incr...
{"title":"Effects of pretreatment with skf‐525a, n‐methyl‐2‐thioimidazole, sodium phenobarbital, or 3‐methylcholanthrene on ethylenethiourea‐induced teratogenicity in hamsters","authors":"K. S. Khera, C. Whalen, F. Iverson","doi":"10.1080/15287398309530342","DOIUrl":"https://doi.org/10.1080/15287398309530342","url":null,"abstract":"Teratogenicity of ethylenethiourea (ETU) was studied in the hamster to define the organ most vulnerable to its teratogenic action. A single intragastric dose of 600, 1200, 1800 or 2400 mg ETU/kg was given in 1.5% aqueous gelatin on d 11 of pregnancy. None of these dose levels produced any apparent maternal toxicity. However, fetal toxicity was apparent in the form of deaths, reduced body weight at the 2400 mg/kg dose, and dose‐related incidences of hydrocephalus, hypoplastic cerebellum, cleft palate, delayed calvarial ossification, and ectrodactyly. The ventricular system of the brain and the cerebellum were among the most sensitive sites for malformations. Effects of metabolic modifiers on the teratogenicity of ETU were studied in separate experiments. Doses of ETU were administered by gastric intubation on d 11 of pregnancy either immediately after an intragastric dose of 200 or 400 mg N‐methyl‐2‐thioimidazole/kg, or 1 h after an ip 40‐mg/kg dose of SKF‐525A. The SKF‐525A pretreatment significantly incr...","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82587211","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}
Pub Date : 1983-02-01DOI: 10.1080/15287398309530339
P. Stromberg, J. Ferrante, S. D. Carter
Seventy‐six fathead minnows were exposed to 12 ppm cadmium for 96‐ h and examined histologically at 1‐wk intervals for 30 d. Thirteen fish (17.1%) died during the exposure period. Lesions associated with acute cadmium toxicity were epithelial necrosis of the skin, oral cavity, gills, olfactory organs, kidney, urinary bladder, ureters, gastrointestinal tract, and hemopoietic organ. The lesions were most severe in fish which died. Survivors had similar but less severe and less extensive lesions. Residual minimal to mild multifocal necrosis was observed In gastrointestinal, branchial epithelium and and hemopoietic tissue up to 29 d postexposure. Radiotracer studies in 50 fish using 115Cd demonstrated a rapid uptake and two phase elimination of cadmium by the fish. Rapid elimination of cadmium occurred within 7 wk and was correlated with lesions in the urinary epithelium. Slow phase elimination occurred for at least 3 wk and was correlated with persistant minimal necrosis in several tissues.
{"title":"Pathology of lethal and sublethal exposure of fathead minnows, pimephales promelas, to cadmium: A model for aquatic toxicity assessment","authors":"P. Stromberg, J. Ferrante, S. D. Carter","doi":"10.1080/15287398309530339","DOIUrl":"https://doi.org/10.1080/15287398309530339","url":null,"abstract":"Seventy‐six fathead minnows were exposed to 12 ppm cadmium for 96‐ h and examined histologically at 1‐wk intervals for 30 d. Thirteen fish (17.1%) died during the exposure period. Lesions associated with acute cadmium toxicity were epithelial necrosis of the skin, oral cavity, gills, olfactory organs, kidney, urinary bladder, ureters, gastrointestinal tract, and hemopoietic organ. The lesions were most severe in fish which died. Survivors had similar but less severe and less extensive lesions. Residual minimal to mild multifocal necrosis was observed In gastrointestinal, branchial epithelium and and hemopoietic tissue up to 29 d postexposure. Radiotracer studies in 50 fish using 115Cd demonstrated a rapid uptake and two phase elimination of cadmium by the fish. Rapid elimination of cadmium occurred within 7 wk and was correlated with lesions in the urinary epithelium. Slow phase elimination occurred for at least 3 wk and was correlated with persistant minimal necrosis in several tissues.","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83622547","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}
Pub Date : 1983-02-01DOI: 10.1080/15287398309530340
E. B. Benson, D. Lange, J. Fujimoto, T. Ishii
Following a 10‐min near‐field exposure to sham radiation of 2.45 GHz microwave (MW) radiation at a power density of 10 mW/cm2, male Swiss‐Cox mice were injected with sodium phenobarbital (PB) (150 mg/kg, iv) and the onset and duration of PB‐induced sleep were recorded. MW‐pretreated mice exhibited a decreased PB sleep onset relative to sham when PB was administered 1 to 45 min following irradiation; however, no effect was seen by 24 h. The duration of PB‐induced sleep was increased; however MW pretreatment did not affect the duration of hexobarbital‐ or pento‐barbital‐induced sleep. At the time of onset of PB‐induced sleep, PB concentrations in brain of MW‐irradiated and control groups were the same despite a twofold difference in the time to sleep onset between these groups. But, when measured 5 min following PB injection, the PB concentrations in brain were higher in MW‐pretreated mice, suggesting that a dispositional mechanism accounted for the observed MW effects on PB‐induced sleep. Mice heated for 1...
{"title":"Effects of acute microwave irradiation on phenobarbital sleep and disposition to brain in mice","authors":"E. B. Benson, D. Lange, J. Fujimoto, T. Ishii","doi":"10.1080/15287398309530340","DOIUrl":"https://doi.org/10.1080/15287398309530340","url":null,"abstract":"Following a 10‐min near‐field exposure to sham radiation of 2.45 GHz microwave (MW) radiation at a power density of 10 mW/cm2, male Swiss‐Cox mice were injected with sodium phenobarbital (PB) (150 mg/kg, iv) and the onset and duration of PB‐induced sleep were recorded. MW‐pretreated mice exhibited a decreased PB sleep onset relative to sham when PB was administered 1 to 45 min following irradiation; however, no effect was seen by 24 h. The duration of PB‐induced sleep was increased; however MW pretreatment did not affect the duration of hexobarbital‐ or pento‐barbital‐induced sleep. At the time of onset of PB‐induced sleep, PB concentrations in brain of MW‐irradiated and control groups were the same despite a twofold difference in the time to sleep onset between these groups. But, when measured 5 min following PB injection, the PB concentrations in brain were higher in MW‐pretreated mice, suggesting that a dispositional mechanism accounted for the observed MW effects on PB‐induced sleep. Mice heated for 1...","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82370752","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}
Pub Date : 1983-02-01DOI: 10.1080/15287398309530344
C. Farr, C. Aldous, Raghubir P. Sharma
Sprague‐Dawley‐derived rats were fed doses of tri‐o‐tolyl phosphate (TOTP) via gavage. The dose levels and administration periods were established in previous experiments designed to assess clinical neuropathy using rats trained to walk on a rotorod apparatus fitted with an electrode floor. After intravenous injections of either [3H]tryptophan or [3H]tyrosine, whole‐rat‐brain homogenates were analyzed, using liquid scintillation and spectrofluorometric techniques, for specific activities and levels of endogenous brain amines and their metabolites. Serotonin, norephinephrine, and dopamine turnover rates were calculated using specific activities obtained at two different sacrifice time periods. Animals given 6 doses of 30–300 mg TOTP/kg body weight, administered every 3 d, showed slightly elevated, nonsignificant serotonin turnover rates, while levels of serotonin and tryptophan remained unchanged with a slight decrease in 4‐hydroxyindoleacetic acid levels at the highest dosages. Similarly treated animals s...
通过灌胃给Sprague - Dawley衍生的大鼠喂食三- o -甲基磷酸(TOTP)。剂量水平和给药周期是在先前的实验中确定的，这些实验旨在评估临床神经病变，实验用的是训练大鼠在装有电极地板的旋转杆装置上行走。静脉注射[3H]色氨酸或[3H]酪氨酸后，使用液体闪烁和荧光光谱技术分析全鼠脑匀浆，以测定内源性脑胺及其代谢物的特定活性和水平。血清素、去甲肾上腺素和多巴胺的周转率是通过在两个不同的牺牲时间段获得的特定活性来计算的。每3天给药6次30-300 mg TOTP/kg体重的动物，血清素周转率略有升高，但不显著，而血清素和色氨酸水平保持不变，4 -羟基吲哚乙酸水平在最高剂量时略有下降。类似对待的动物……
{"title":"Effects of tri‐o‐tolyl phosphate on rat brain catecholamine and indoleamine metabolism","authors":"C. Farr, C. Aldous, Raghubir P. Sharma","doi":"10.1080/15287398309530344","DOIUrl":"https://doi.org/10.1080/15287398309530344","url":null,"abstract":"Sprague‐Dawley‐derived rats were fed doses of tri‐o‐tolyl phosphate (TOTP) via gavage. The dose levels and administration periods were established in previous experiments designed to assess clinical neuropathy using rats trained to walk on a rotorod apparatus fitted with an electrode floor. After intravenous injections of either [3H]tryptophan or [3H]tyrosine, whole‐rat‐brain homogenates were analyzed, using liquid scintillation and spectrofluorometric techniques, for specific activities and levels of endogenous brain amines and their metabolites. Serotonin, norephinephrine, and dopamine turnover rates were calculated using specific activities obtained at two different sacrifice time periods. Animals given 6 doses of 30–300 mg TOTP/kg body weight, administered every 3 d, showed slightly elevated, nonsignificant serotonin turnover rates, while levels of serotonin and tryptophan remained unchanged with a slight decrease in 4‐hydroxyindoleacetic acid levels at the highest dosages. Similarly treated animals s...","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79462263","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}
Pub Date : 1983-02-01DOI: 10.1080/15287398309530343
C. Grabowski, D. B. Payne
Prenatal exposure to mirex induces a high rate of perinatal death without obvious cause. Part I of this study (Grabowski and Payne, 1982), in which fetuses were exposed to a moderate dose of mirex and observed just prior to parturition, it was found that 14% had died recently and an additional 9% were apparently dying with serious cardiovascular symptoms. In the present study, electrocardiograms of normal (oil‐fed controls) and mirex‐exposed rats (6 mg/kg·d of insecticide on d 8 to 15 of gestation) were obtained at birth and for several days afterwards. An ECG was obtained from most individuals within 5 min of birth. Pups were then weighed and tattooed so that individuals could be followed to postnatal d 5. Data on 70 control newborns were compared with that on 131 mirex‐treated pups. In the treated group, 23% were stillborn. Of those born alive, 8% died within 6 h of birth, and another 13% within 48 h. At birth, 14% had first‐degree heart blocks, and 2% had second‐degree blocks. All of those with second‐...
{"title":"The causes of perinatal death induced by prenatal exposure of rats to the pesticide, mirex. part II: Postnatal observations","authors":"C. Grabowski, D. B. Payne","doi":"10.1080/15287398309530343","DOIUrl":"https://doi.org/10.1080/15287398309530343","url":null,"abstract":"Prenatal exposure to mirex induces a high rate of perinatal death without obvious cause. Part I of this study (Grabowski and Payne, 1982), in which fetuses were exposed to a moderate dose of mirex and observed just prior to parturition, it was found that 14% had died recently and an additional 9% were apparently dying with serious cardiovascular symptoms. In the present study, electrocardiograms of normal (oil‐fed controls) and mirex‐exposed rats (6 mg/kg·d of insecticide on d 8 to 15 of gestation) were obtained at birth and for several days afterwards. An ECG was obtained from most individuals within 5 min of birth. Pups were then weighed and tattooed so that individuals could be followed to postnatal d 5. Data on 70 control newborns were compared with that on 131 mirex‐treated pups. In the treated group, 23% were stillborn. Of those born alive, 8% died within 6 h of birth, and another 13% within 48 h. At birth, 14% had first‐degree heart blocks, and 2% had second‐degree blocks. All of those with second‐...","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75606690","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}
Pub Date : 1983-02-01DOI: 10.1080/15287398309530337
E. Uyeki, A. Nishio
Potassium dichromate [Cr(VI), hexavalent chromium] and chromic chloride [Cr(III), trivalent chromium] were added to tissue cultures of Chinese hamster ovary (CHO) cells. Cr(III) at 10 μM did not significantly affect cell proliferation. On the other hand, 10 and 1 μM Cr(VI) inhibited cell proliferation, while 0.1 μM did not. Addition of ascorbic acid (50 μg/ml), for periods up to 6 h after Cr(VI), effectively reversed the antiproliferative effects of Cr(VI). Several sulfhydryl‐containing agents, under similar conditions, were ineffective. Cr(III) at 10 μM did not induce sister chromatid exchanges (SCEs) in cultured CHO cells. On the other hand, Cr(VI) did; there was a dose‐response in the SCE induction by Cr(VI) between 0.01 and 1 μM Cr(VI). Addition of ascorbic acid, for periods up to 4 h after Cr(VI), reversed Cr(VI)‐induced SCEs. We suggest that the genotoxic effects of Cr(VI) (i.e., SCE induction) may be causally related to the antiproliferative effects that we observed.
{"title":"Antiproliferative and genotoxic effects of chromium on cultured mammalian cells","authors":"E. Uyeki, A. Nishio","doi":"10.1080/15287398309530337","DOIUrl":"https://doi.org/10.1080/15287398309530337","url":null,"abstract":"Potassium dichromate [Cr(VI), hexavalent chromium] and chromic chloride [Cr(III), trivalent chromium] were added to tissue cultures of Chinese hamster ovary (CHO) cells. Cr(III) at 10 μM did not significantly affect cell proliferation. On the other hand, 10 and 1 μM Cr(VI) inhibited cell proliferation, while 0.1 μM did not. Addition of ascorbic acid (50 μg/ml), for periods up to 6 h after Cr(VI), effectively reversed the antiproliferative effects of Cr(VI). Several sulfhydryl‐containing agents, under similar conditions, were ineffective. Cr(III) at 10 μM did not induce sister chromatid exchanges (SCEs) in cultured CHO cells. On the other hand, Cr(VI) did; there was a dose‐response in the SCE induction by Cr(VI) between 0.01 and 1 μM Cr(VI). Addition of ascorbic acid, for periods up to 4 h after Cr(VI), reversed Cr(VI)‐induced SCEs. We suggest that the genotoxic effects of Cr(VI) (i.e., SCE induction) may be causally related to the antiproliferative effects that we observed.","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90572775","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}
Pub Date : 1983-02-01DOI: 10.1080/15287398309530341
A. G. Braun, P. B. Horowicz
To gain experience in the in vitro assay of environmental teratogens, 32 pesticides and TCDD have been tested for their ability to Inhibit tumor cells attachment to polyethylene disks coated with concanavalin A. Of 25 pesticides that inhibited attachment, 23 (92%) have been reported to be teratogenic in mammals or avians. From a qualitative viewpoint, agents that inhibit attachment in vitro are very likely to be teratogenic in vivo. There was a quantitative correlation between the inhibitory activity and the lowest reported teratogenic dose in chick embryo for nine pesticides. However, no similar correlation between inhibitory concentration, in vitro, and mammalian teratogenicity was found. Presumably maternal effects of absorption, metabolism, and distribution distort the relationship between the dose administered to the mother and the concentration of teratogenic agent at target embryonic tissues. Lack of inhibition in vitro did not indicate lack of teratogenicity, as five of eight noninhibitory agents ...
{"title":"Lectin‐mediated attachment assay for teratogens: Results with 32 pesticides","authors":"A. G. Braun, P. B. Horowicz","doi":"10.1080/15287398309530341","DOIUrl":"https://doi.org/10.1080/15287398309530341","url":null,"abstract":"To gain experience in the in vitro assay of environmental teratogens, 32 pesticides and TCDD have been tested for their ability to Inhibit tumor cells attachment to polyethylene disks coated with concanavalin A. Of 25 pesticides that inhibited attachment, 23 (92%) have been reported to be teratogenic in mammals or avians. From a qualitative viewpoint, agents that inhibit attachment in vitro are very likely to be teratogenic in vivo. There was a quantitative correlation between the inhibitory activity and the lowest reported teratogenic dose in chick embryo for nine pesticides. However, no similar correlation between inhibitory concentration, in vitro, and mammalian teratogenicity was found. Presumably maternal effects of absorption, metabolism, and distribution distort the relationship between the dose administered to the mother and the concentration of teratogenic agent at target embryonic tissues. Lack of inhibition in vitro did not indicate lack of teratogenicity, as five of eight noninhibitory agents ...","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83072376","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}
Pub Date : 1983-02-01DOI: 10.1080/15287398309530333
G. Meadows, A. Palacio
The toxicity of long‐term exposure to Mount St. Helens volcanic ash was studied in female B6D2F1 mice. The mice, fed diets containing 10% ash, were observed for 43 wk. Exposure had no effect on hematology, plasma amino acid levels, food and water consumption, and urinary and fecal output. Mice fed the ash diet grew at a faster rate than mice maintained on the control diet. This increase was reflected in an increase in carcass and gastrointestinal tract weight. Lactic dehydrogenase was elevated throughout the observation period, but other clinical chemistries were normal. Mice suffered no apparent respiratory problems during the 43‐wk observation period. The ash had mixed effects on survival of B16 melanoma‐bearing mice. Sudden exposure and long‐term exposure (30 and 44 wk) in mice injected with a rapidly growing tumor did not affect survival. In contrast, mice implanted with a slow‐growing tumor at 7 and 15 wk of exposure exhibited decreased survival relative to control mice.
{"title":"Long‐term effects of volcanic ash from Mount St. Helens in normal and melanoma‐bearing mice","authors":"G. Meadows, A. Palacio","doi":"10.1080/15287398309530333","DOIUrl":"https://doi.org/10.1080/15287398309530333","url":null,"abstract":"The toxicity of long‐term exposure to Mount St. Helens volcanic ash was studied in female B6D2F1 mice. The mice, fed diets containing 10% ash, were observed for 43 wk. Exposure had no effect on hematology, plasma amino acid levels, food and water consumption, and urinary and fecal output. Mice fed the ash diet grew at a faster rate than mice maintained on the control diet. This increase was reflected in an increase in carcass and gastrointestinal tract weight. Lactic dehydrogenase was elevated throughout the observation period, but other clinical chemistries were normal. Mice suffered no apparent respiratory problems during the 43‐wk observation period. The ash had mixed effects on survival of B16 melanoma‐bearing mice. Sudden exposure and long‐term exposure (30 and 44 wk) in mice injected with a rapidly growing tumor did not affect survival. In contrast, mice implanted with a slow‐growing tumor at 7 and 15 wk of exposure exhibited decreased survival relative to control mice.","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79364182","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}
Pub Date : 1983-02-01DOI: 10.1080/15287398309530336
R. Bull
Rat pups taken from dams exposed to lead (Pb) at concentrations of 0, 5, 30, and 200 mg/l of drinking water from 14 d prior to breeding to 21 d postpartum display evidence of delayed maturation of the cerebral cortex. Delayed maturation was observed as an alteration in the ontogeny of metabolic responses of isolated cerebral tissues taken from rat pups of Pb‐treated dams to elevated K+ concentrations. These responses were found to undergo substantial developmental changes between 6 and 50 d of postnatal age. The delay in development was most marked with respect to the development of the late reduction of NAD(P)1, which occurs in response to an increase of media K+ concentration from 3 to 30 mM. Delays in the development of this response were observed as late as 50 d of age, but assumed the adult pattern by 90 d of age. An increased uptake of oxygen in response to an elevated concentration of K+ provided evidence of metabolic uncoupling in tissues taken from animals at 15 and 21 d of age. At 15 d of age, i...
{"title":"Delayed metabolic maturation of the cerebral cortex of rat pups derived from lead‐treated dams","authors":"R. Bull","doi":"10.1080/15287398309530336","DOIUrl":"https://doi.org/10.1080/15287398309530336","url":null,"abstract":"Rat pups taken from dams exposed to lead (Pb) at concentrations of 0, 5, 30, and 200 mg/l of drinking water from 14 d prior to breeding to 21 d postpartum display evidence of delayed maturation of the cerebral cortex. Delayed maturation was observed as an alteration in the ontogeny of metabolic responses of isolated cerebral tissues taken from rat pups of Pb‐treated dams to elevated K+ concentrations. These responses were found to undergo substantial developmental changes between 6 and 50 d of postnatal age. The delay in development was most marked with respect to the development of the late reduction of NAD(P)1, which occurs in response to an increase of media K+ concentration from 3 to 30 mM. Delays in the development of this response were observed as late as 50 d of age, but assumed the adult pattern by 90 d of age. An increased uptake of oxygen in response to an elevated concentration of K+ provided evidence of metabolic uncoupling in tissues taken from animals at 15 and 21 d of age. At 15 d of age, i...","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81537250","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}
Pub Date : 1983-02-01DOI: 10.1080/15287398309530338
M. Basinger, R. Forti, L. T. Burka, M. M. Jones, W. Mitchell, Joyce E. Johnson, S. Gibbs
Nine phenolic chelating agents were examined as antidotes for acute uranyl acetate intoxication. The ability of these compounds to promote survival was determined and the ability of two of them to remove uranium from the liver and kidney was compared with that of Na3 CaDTPA. The most effective compounds of this type in promoting survival were found to be Tiron and p‐aminosalicylic acid, but Tiron was much more effective in decreasing the uranium burden of the liver and kidneys. These compounds exhibit an antidotal action at higher uranium levels than the compounds reported in earlier studies. The compounds all seem to possess a very modest toxicity when administered ip.
{"title":"Phenolic chelating agents as antidotes for acute uranyl acetate intoxication in mice","authors":"M. Basinger, R. Forti, L. T. Burka, M. M. Jones, W. Mitchell, Joyce E. Johnson, S. Gibbs","doi":"10.1080/15287398309530338","DOIUrl":"https://doi.org/10.1080/15287398309530338","url":null,"abstract":"Nine phenolic chelating agents were examined as antidotes for acute uranyl acetate intoxication. The ability of these compounds to promote survival was determined and the ability of two of them to remove uranium from the liver and kidney was compared with that of Na3 CaDTPA. The most effective compounds of this type in promoting survival were found to be Tiron and p‐aminosalicylic acid, but Tiron was much more effective in decreasing the uranium burden of the liver and kidneys. These compounds exhibit an antidotal action at higher uranium levels than the compounds reported in earlier studies. The compounds all seem to possess a very modest toxicity when administered ip.","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76363811","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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