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Year: 2010 Publisher: Lyon (FR) : International Agency for Research on Cancer,
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Year: 2021 Publisher: North Carolina, USA : National Toxicology Program (U.S.),
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PERINATAL AND THREE-MONTH STUDY IN RATS: Beginning on GDs6, groups of eight F0stime-mated female rats were exposed to ST in drinking water throughout gestation and lactation at one of five exposure concentrations (125, 250, 500, 1,000, or 2,000smg/L) or were provided the vehicle control (deionized water). Groups of 10 F1srats per sex continued on in the study after weaning and were given drinking water containing the same respective ST concentrations for 3smonths. There were no significant effects of ST exposure on pregnancy status, maternal survival, or littering parameters. By the end of lactation, dams in the 1,000 and 2,000smg/L groups showed significant decreases in group mean body weight of approximately 10% and 18%, respectively, and water consumption was significantly decreased for the 500, 1,000, and 2,000smg/L groups relative to the vehicle control group over the LDs17 to LDs21 interval. When adjusted for litter size, the mean body weight of male and female pups in the 2,000smg/L group on PNDs21 was significantly decreased by approximately 16% and 11%, respectively, compared to the corresponding vehicle control groups. There were no early deaths during the 3-month study. When compared to the vehicle control group, final mean body weights were lower for the 1,000 and 2,000smg/L males and 2,000 mg/L females. Water consumption was lower for the 1,000 and 2,000smg/L males and females. The urine xanthine/creatinine ratios were significantly increased in all male and female exposed groups. Serum insulin concentrations were significantly decreased in the 2,000smg/L males relative to the vehicle control males. Significantly decreased absolute weights were observed in several organs but were considered secondary to body weights reductions. Exposure-related histological lesions were limited to the kidneys and included increased incidences of renal tubule regeneration in the 1,000 and 2,000smg/L males and females; the increases in the 2,000smg/L groups were significant relative to the vehicle control group. CONCLUSIONS: Under the conditions of these 2-year drinking water studies, there was no evidence of carcinogenic activity of sodium tungstate dihydrate (ST) in male Hsd:Sprague Dawley(r) SD(r) rats at exposure concentrations of 250, 500, or 1,000smg/L. There was equivocal evidence of carcinogenic activity of ST in female Hsd:Sprague Dawley(r) SD(r) rats based on increased incidences of C-cell adenoma or carcinoma (combined) of the thyroid gland. There was equivocal evidence of carcinogenic activity of ST in male B6C3F1/N mice based on the occurrences of renal tubule adenoma or carcinoma (combined) in exposed animals. There was no evidence of carcinogenic activity of ST in female B6C3F1/N mice at exposure concentrations of 500, 1,000, or 2,000smg/L. Exposure to ST in drinking water caused increased incidences of nonneoplastic lesions in the kidney of male and female rats and mice, in the uterus of female rats, in the large intestine of male and female mice, and in the testes of male mice.SYNONYMS: Tungstic acid sodium salt dehydrate.
Book
Year: 2021 Publisher: North Carolina, USA : National Toxicology Program,
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PERINATAL AND POSTWEANING STUDY IN RATS (STUDYS1): During the perinatal period, lower maternal mean body weight, maternal mean body weight gain, and feed consumption were observed in F0sdams exposed to 10,000 ppm DEHP relative to control animals. Also in that exposure group, litter size and pup weights on PNDs1 were significantly decreased compared to the control group. Male and female pup mean body weight gains were significantly decreased in the 10,000sppm group during lactation and resulted in significantly decreased pup body weights at weaning when compared to the control group. Pup survival was not affected following gestational and lactational DEHP exposure. Following perinatal and 2syears of postweaning DEHP exposure, survival of exposed male and female rats to study termination was similar to that of control groups; however, there were decreases in mean body weight in the 10,000sppm group compared to the control group. Significant increases in the incidences of hepatocellular adenoma, hepatocellular adenoma or carcinoma (combined), pancreatic acinar adenoma, and pancreatic acinar adenoma or carcinoma (combined) were observed in the 3,000 and 10,000sppm male rats relative to the control group. Higher incidences of hepatocellular carcinomas (10,000sppm males) and pancreatic acinar carcinomas (3,000sppm males) were also observed. In female rats, significant increases in the incidences of liver neoplasms occurred in the 3,000sppm (hepatocellular adenoma and hepatocellular adenoma or carcinoma [combined]) and 10,000sppm (hepatocellular carcinoma and hepatocellular adenoma or carcinoma [combined]) groups. Occurrences of pancreatic acinar adenomas were observed in the 3,000 and 10,000sppm female groups, and a trend of higher incidence of uterine adenocarcinomas with increasing exposure was observed given the incidence in the 10,000sppm group. Nonneoplastic lesions were observed in the liver (male and female), pancreas (female), testis, epididymis, kidney (male and female), heart (male only), bone marrow (male only), and pituitary gland (male only). CONCLUSIONS: Under the conditions of the perinatal and postweaning feed study (Studys1), there was clear evidence of carcinogenic activity of di(2-ethylhexyl) phthalate (DEHP) in male Hsd:Sprague Dawley(r) SD(r) rats based on the increased incidences of hepatocellular adenoma or carcinoma (combined) and acinar adenoma or carcinoma (combined) neoplasms (predominately adenomas) of the pancreas. There was clear evidence of carcinogenic activity of DEHP in female Hsd:Sprague Dawley(r) SD(r) rats based on the increased incidence of hepatocellular adenoma or carcinoma (combined). The occurrence of pancreatic acinar adenoma or carcinoma (combined) was considered to be related to exposure. The occurrence of uterine (including cervix) adenoma, adenocarcinoma, squamous cell carcinoma, or squamous cell papilloma (combined) in female rats may have been related to exposure. Under the conditions of the postweaning-only feed study (Studys2), there was clear evidence of carcinogenic activity of DEHP in male Hsd:Sprague Dawley(r) SD(r) rats based on the increased incidences of hepatocellular adenoma or carcinoma (combined) and acinar adenoma or carcinoma (combined) neoplasms (predominately adenomas) of the pancreas. The occurrence of testicular interstitial cell adenoma in male rats may have been related to exposure. There was clear evidence of carcinogenic activity of DEHP in female Hsd:Sprague Dawley(r) SD(r) rats based on the increased incidences of hepatocellular adenoma or carcinoma (combined) and uterine (including cervix) adenoma, adenocarcinoma, squamous cell carcinoma, or squamous cell papilloma (combined). The occurrence of pancreatic acinar adenoma or carcinoma (combined) in female rats was considered to be related to exposure. The BMD analysis shows there was no consistent pattern indicating that perinatal and postweaning exposure was more sensitive compared to postweaning-only exposure and modeled responses were within threefold of each other. However, there was a stronger carcinogenic response in the reproductive organs (uterus and testis) in the postweaning-only exposure study compared to the perinatal and postweaning exposure study. Perinatal and postweaning exposure to DEHP (Studys1) resulted in increased incidence of nonneoplastic lesions in the liver, kidney, heart (male), pancreas (female), pituitary gland (male), bone marrow (male), testis, and epididymis. In addition, exposure increased gross lesions within the reproductive tract of males and females. Postweaning exposure to DEHP (Studys2) resulted in increased incidence of nonneoplastic lesions in the liver, pancreas, heart (male), pituitary gland (male), bone marrow (male), testis, epididymis, and uterus.SYNONYMS: Bis(2-ethylhexyl)phthalate; dioctyl phthalate; phthalic acid di(2-ethylhexyl) ester; bis(2-ethylhexyl) 1,2-benzenedicarboxylate; 1,2-benzenedicarboxylic acid bis(2-ethylhexyl) ester TRADE NAMES: Platinol DOP; Octoil; Silicol 150; Bisoflex 81; Eviplast 80.
Book
Year: 1978 Publisher: Bethesda, Md. : U.S. Dept. of Health, Education, and Welfare, Public Health Service, National Institutes of Health,
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Book
Year: 2020 Publisher: Lyon (FR) : International Agency for Research on Cancer,
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Book
Year: 1973 Publisher: Stockholm,
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Book
Year: 2020 Publisher: Lyon (FR) : International Agency for Research on Cancer,
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Book
Year: 2021 Publisher: North Carolina, USA : National Toxicology Program (U.S.),
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PERINATAL AND THREE-MONTH STUDY IN RATS: Beginning on GDs6, groups of eight F0stime-mated female rats were exposed to ST in drinking water throughout gestation and lactation at one of five exposure concentrations (125, 250, 500, 1,000, or 2,000smg/L) or were provided the vehicle control (deionized water). Groups of 10 F1srats per sex continued on in the study after weaning and were given drinking water containing the same respective ST concentrations for 3smonths. There were no significant effects of ST exposure on pregnancy status, maternal survival, or littering parameters. By the end of lactation, dams in the 1,000 and 2,000smg/L groups showed significant decreases in group mean body weight of approximately 10% and 18%, respectively, and water consumption was significantly decreased for the 500, 1,000, and 2,000smg/L groups relative to the vehicle control group over the LDs17 to LDs21 interval. When adjusted for litter size, the mean body weight of male and female pups in the 2,000smg/L group on PNDs21 was significantly decreased by approximately 16% and 11%, respectively, compared to the corresponding vehicle control groups. There were no early deaths during the 3-month study. When compared to the vehicle control group, final mean body weights were lower for the 1,000 and 2,000smg/L males and 2,000 mg/L females. Water consumption was lower for the 1,000 and 2,000smg/L males and females. The urine xanthine/creatinine ratios were significantly increased in all male and female exposed groups. Serum insulin concentrations were significantly decreased in the 2,000smg/L males relative to the vehicle control males. Significantly decreased absolute weights were observed in several organs but were considered secondary to body weights reductions. Exposure-related histological lesions were limited to the kidneys and included increased incidences of renal tubule regeneration in the 1,000 and 2,000smg/L males and females; the increases in the 2,000smg/L groups were significant relative to the vehicle control group. CONCLUSIONS: Under the conditions of these 2-year drinking water studies, there was no evidence of carcinogenic activity of sodium tungstate dihydrate (ST) in male Hsd:Sprague Dawley(r) SD(r) rats at exposure concentrations of 250, 500, or 1,000smg/L. There was equivocal evidence of carcinogenic activity of ST in female Hsd:Sprague Dawley(r) SD(r) rats based on increased incidences of C-cell adenoma or carcinoma (combined) of the thyroid gland. There was equivocal evidence of carcinogenic activity of ST in male B6C3F1/N mice based on the occurrences of renal tubule adenoma or carcinoma (combined) in exposed animals. There was no evidence of carcinogenic activity of ST in female B6C3F1/N mice at exposure concentrations of 500, 1,000, or 2,000smg/L. Exposure to ST in drinking water caused increased incidences of nonneoplastic lesions in the kidney of male and female rats and mice, in the uterus of female rats, in the large intestine of male and female mice, and in the testes of male mice.SYNONYMS: Tungstic acid sodium salt dehydrate.
Book
Year: 2021 Publisher: North Carolina, USA : National Toxicology Program,
Abstract | Keywords | Export | Availability | Bookmark
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PERINATAL AND POSTWEANING STUDY IN RATS (STUDYS1): During the perinatal period, lower maternal mean body weight, maternal mean body weight gain, and feed consumption were observed in F0sdams exposed to 10,000 ppm DEHP relative to control animals. Also in that exposure group, litter size and pup weights on PNDs1 were significantly decreased compared to the control group. Male and female pup mean body weight gains were significantly decreased in the 10,000sppm group during lactation and resulted in significantly decreased pup body weights at weaning when compared to the control group. Pup survival was not affected following gestational and lactational DEHP exposure. Following perinatal and 2syears of postweaning DEHP exposure, survival of exposed male and female rats to study termination was similar to that of control groups; however, there were decreases in mean body weight in the 10,000sppm group compared to the control group. Significant increases in the incidences of hepatocellular adenoma, hepatocellular adenoma or carcinoma (combined), pancreatic acinar adenoma, and pancreatic acinar adenoma or carcinoma (combined) were observed in the 3,000 and 10,000sppm male rats relative to the control group. Higher incidences of hepatocellular carcinomas (10,000sppm males) and pancreatic acinar carcinomas (3,000sppm males) were also observed. In female rats, significant increases in the incidences of liver neoplasms occurred in the 3,000sppm (hepatocellular adenoma and hepatocellular adenoma or carcinoma [combined]) and 10,000sppm (hepatocellular carcinoma and hepatocellular adenoma or carcinoma [combined]) groups. Occurrences of pancreatic acinar adenomas were observed in the 3,000 and 10,000sppm female groups, and a trend of higher incidence of uterine adenocarcinomas with increasing exposure was observed given the incidence in the 10,000sppm group. Nonneoplastic lesions were observed in the liver (male and female), pancreas (female), testis, epididymis, kidney (male and female), heart (male only), bone marrow (male only), and pituitary gland (male only). CONCLUSIONS: Under the conditions of the perinatal and postweaning feed study (Studys1), there was clear evidence of carcinogenic activity of di(2-ethylhexyl) phthalate (DEHP) in male Hsd:Sprague Dawley(r) SD(r) rats based on the increased incidences of hepatocellular adenoma or carcinoma (combined) and acinar adenoma or carcinoma (combined) neoplasms (predominately adenomas) of the pancreas. There was clear evidence of carcinogenic activity of DEHP in female Hsd:Sprague Dawley(r) SD(r) rats based on the increased incidence of hepatocellular adenoma or carcinoma (combined). The occurrence of pancreatic acinar adenoma or carcinoma (combined) was considered to be related to exposure. The occurrence of uterine (including cervix) adenoma, adenocarcinoma, squamous cell carcinoma, or squamous cell papilloma (combined) in female rats may have been related to exposure. Under the conditions of the postweaning-only feed study (Studys2), there was clear evidence of carcinogenic activity of DEHP in male Hsd:Sprague Dawley(r) SD(r) rats based on the increased incidences of hepatocellular adenoma or carcinoma (combined) and acinar adenoma or carcinoma (combined) neoplasms (predominately adenomas) of the pancreas. The occurrence of testicular interstitial cell adenoma in male rats may have been related to exposure. There was clear evidence of carcinogenic activity of DEHP in female Hsd:Sprague Dawley(r) SD(r) rats based on the increased incidences of hepatocellular adenoma or carcinoma (combined) and uterine (including cervix) adenoma, adenocarcinoma, squamous cell carcinoma, or squamous cell papilloma (combined). The occurrence of pancreatic acinar adenoma or carcinoma (combined) in female rats was considered to be related to exposure. The BMD analysis shows there was no consistent pattern indicating that perinatal and postweaning exposure was more sensitive compared to postweaning-only exposure and modeled responses were within threefold of each other. However, there was a stronger carcinogenic response in the reproductive organs (uterus and testis) in the postweaning-only exposure study compared to the perinatal and postweaning exposure study. Perinatal and postweaning exposure to DEHP (Studys1) resulted in increased incidence of nonneoplastic lesions in the liver, kidney, heart (male), pancreas (female), pituitary gland (male), bone marrow (male), testis, and epididymis. In addition, exposure increased gross lesions within the reproductive tract of males and females. Postweaning exposure to DEHP (Studys2) resulted in increased incidence of nonneoplastic lesions in the liver, pancreas, heart (male), pituitary gland (male), bone marrow (male), testis, epididymis, and uterus.SYNONYMS: Bis(2-ethylhexyl)phthalate; dioctyl phthalate; phthalic acid di(2-ethylhexyl) ester; bis(2-ethylhexyl) 1,2-benzenedicarboxylate; 1,2-benzenedicarboxylic acid bis(2-ethylhexyl) ester TRADE NAMES: Platinol DOP; Octoil; Silicol 150; Bisoflex 81; Eviplast 80.
Book
Year: 2010 Publisher: Lyon (FR) : International Agency for Research on Cancer,
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