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M J Appel - One of the best experts on this subject based on the ideXlab platform.
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Effect of D-tagatose on Liver Weight and glycogen content of rats.
Regulatory toxicology and pharmacology : RTP, 1999Co-Authors: A Bär, B A Lina, D M De Groot, B De Bie, M J AppelAbstract:D-tagatose is an incompletely absorbed ketohexose (stereoisomer of D-fructose) which has potential as an energy-reduced alternative sweetener. In an earlier 90-day toxicity study, rats fed diets with 10, 15 and 20% D-tagatose exhibited increased Liver Weights, but no histopathological alterations. To determine whether there might be any toxicological relevance to this effect, three studies were conducted in male, adult Sprague-Dawley rats. In the first study, four groups received Purina diet (group A), Purina diet with 20% D-tagatose (group B), SDS diet (group C), or SDS diet with 20% D-tagatose (group D). For groups A and B, the 28-day treatment period was followed by a 14-day recovery period (Purina diet). Food remained available to all animals until the time of sacrifice. Groups of 10 rats were killed on days 14 (groups A and B), 28 (groups A-D), and 42 (groups A and B). Body Weights, as well as Weights of wet and lyophilized Livers, were determined. The lyophilized Livers collected on day 28 from groups A and B were analyzed for protein, total lipid, glycogen, DNA, and residual moisture. By day 14, relative wet Liver Weights had increased by 23% in group B. On day 28, the increase was 38% in group B and 44% in group D. At the end of the recovery period, the increase had diminished to 14% in group B. On day 28, Liver glycogen content (in %) was significantly increased, and Liver protein, lipid, and DNA contents were significantly decreased in group B compared to group A. Total amounts per Liver of protein, total lipid, glycogen, and DNA were significantly increased. In the second study, four groups of 20 rats each received SDS diet with 0, 5, 10, and 20% D-tagatose for 29-31 days. The food was available until the time of sacrifice. At termination, plasma was obtained from 10 rats/group for clinicochemical analyses. Five rats/group were subjected to whole-body perfusion, followed by processing of Livers for qualitative and quantitative electron microscopic examination. Livers of 6 rats/group were analyzed for acyl-CoA oxidase and laurate 12-hydroxylase (cytochrome P450 4A1) activity, DNA synthesis (Ki-67 index), and number of nuclei per unit area of tissue. Liver Weights were significantly increased in linear relation to the D-tagatose intake. Plasma transaminases (but not glutamyl transferase and alkaline phosphatase) were increased in the high-dose group. Except for glycogen accumulation, no ultrastructural changes were seen on electron microscopic examination of Livers of the control and high-dose groups. Morphometric analysis confirmed the increase of glycogen and the absence of alterations of endoplasmatic reticulum, mitochondria, and Golgi apparatus. The Ki-67 index did not differ between the groups. A dose-related decrease of the number of nuclei per unit area signified some hepatocellular hypertrophy. Acyl-CoA oxidase and CYP4A1 activity were significantly increased in the mid- and high-dose groups, but these increases were small and not accompanied by electron-microscopic evidence of peroxisome proliferation. In the third study, four groups received SDS diet (groups A and C) or SDS diet with 5% D-tagatose (groups B and D). All animals were killed on day 28. Groups A and B were fasted for 24 h before sacrifice; groups C and D had food available until sacrifice. Liver Weights and Liver composition were measured as in Study 1. Relative wet and dry Liver Weights were increased in response to the treatment in rats killed under the fed condition, but not in rats killed under the fasted condition. The Livers of the treated rats (group D) had an increased glycogen content in comparison to the controls (group C). Taken together, these results demonstrate that D-tagatose at dietary levels of 5-20% increases Liver glycogen deposition and relative Liver Weights in nonfasting rats. In fasted rats the 5% dose level is the no-effect level. (ABSTRACT TRUNCATED)
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Effect of D-tagatose on Liver Weight and glycogen content of rats.
Regulatory Toxicology and Pharmacology, 1999Co-Authors: A Bär, B A Lina, D M De Groot, B De Bie, M J AppelAbstract:D-Tagatose is an incompletely absorbed ketohexose (stereoisomer of D-fructose) which has potential as an energy-reduced alternative sweetener. In an earlier 90-day toxicity study, rats fed diets with 10, 15 and 20% D-tagatose exhibited increased Liver Weights, but no histopathological alterations. To determine whether there might be any toxicological relevance to this effect, three studies were conducted in male, adult Sprague-Dawley rats. In the first study, four groups received Purina diet (group A), Purina diet with 20% D-tagatose (group B), SDS diet (group C), or SDS diet with 20% D-tagatose (group D). For groups A and B, the 28-day treatment period was followed by a 14-day recovery period (Purina diet). Food remained available to all animals until the time of sacrifice. Groups of 10 rats were killed on days 14 (groups A and B), 28 (groups A-D), and 42 (groups A and B). Body Weights, as well as Weights of wet and lyophilized Livers, were determined. The lyophilized Livers collected on day 28 from groups A and B were analyzed for protein, total lipid, glycogen, DNA, and residual moisture. By day 14, relative wet Liver Weights had increased by 23% in group B. On day 28, the increase was 38% in group B and 44% in group D. At the end of the recovery period, the increase had diminished to 14% in group B. On day 28, Liver glycogen content (in %) was significantly increased, and Liver protein, lipid, and DNA contents were significantly decreased in group B compared to group A. Total amounts per Liver of protein, total lipid, glycogen, and DNA were significantly increased. In the second study, four groups of 20 rats each received SDS diet with 0, 5, 10, and 20% D-tagatose for 29-31 days. The food was available until the time of sacrifice. At termination, plasma was obtained from 10 rats/group for clinicochemical analyses. Five rats/group were subjected to whole-body perfusion, followed by processing of Livers for qualitative and quantitative electron microscopic examination. Livers of 6 rats/group were analyzed for acyl-CoA oxidase and laurate 12-hydroxylase (cytochrome P450 4A1) activity, DNA synthesis (Ki-67 index), and number of nuclei per unit area of tissue. Liver Weights were significantly increased in linear relation to the D-tagatose intake. Plasma transaminases (but not glutamyl transferase and alkaline phosphatase) were increased in the high-dose group. Except for glycogen accumulation, no ultrastructural changes were seen on electron microscopic examination of Livers of the control and high-dose groups. Morphometric analysis confirmed the increase of glycogen and the absence of alterations of endoplasmatic reticulum, mitochondria, and Golgi apparatus. The Ki-67 index did not differ between the groups. A dose-related decrease of the number of nuclei per unit area signified some hepatocellular hypertrophy. Acyl-CoA oxidase and CYP4A1 activity were significantly increased in the mid- and high-dose groups, but these increases were small and not accompanied by electron-microscopic evidence of peroxisome proliferation. In the third study, four groups received SDS diet (groups A and C) or SDS diet with 5% D-tagatose (groups B and D). All animals were killed on day 28. Groups A and B were fasted for 24 h before sacrifice; groups C and D had food available until sacrifice. Liver Weights and Liver composition were measured as in Study 1. Relative wet and dry Liver Weights were increased in response to the treatment in rats killed under the fed condition, but not in rats killed under the fasted condition. The Livers of the treated rats (group D) had an increased glycogen content in comparison to the controls (group C). Taken together, these results demonstrate that D-tagatose at dietary levels of 5-20% increases Liver glycogen deposition and relative Liver Weights in nonfasting rats. In fasted rats the 5% dose level is the no-effect level. At the higher dose levels, the increased glycogen deposition induced minimal hypertrophy and some compensatory growth which reached completion before the end of the 28-day treatment period. It is concluded that the Liver enlargement seen in response to the consumption of D-tagatose is a physiological response to the treatment-induced increased glycogen deposition. No hepatocellular growth was seen at the 5% dietary level of D-tagatose (corresponding to an intake of 2.6-2.8 g/kg body wt), suggesting that the increase of Liver glycogen at this dose remained within normal limits. © 1999 Academic Press.
Dingxin Long - One of the best experts on this subject based on the ideXlab platform.
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subchronic toxicity of low dose propoxur permethrin and their combination on the redox status of rat Liver
Chemico-Biological Interactions, 2017Co-Authors: Pan Wang, Yujie Liang, Huiping Wang, Yingjian Sun, Dingxin LongAbstract:Carbamates and pyrethroids are widely used pesticides. However, their joint toxicity at low doses with long-term exposure remains unknown. Therefore, we investigated the subchronic joint hepatotoxicity of the two representative pesticides within these two classes, i.e., propoxur (PR) and permethrin (PE) in rats. The male Wistar rats were orally treated with three different doses of PR, PE and their mixtures for 90 consecutive days. Liver Weight, serum clinical chemistry parameters and histopathological changes were measured to access the hepatotoxicity. In addition, oxidative stress markers in Liver were measured using biochemical assays. The results showed that PR reduced Liver Weight and lead to prominent Liver histological changes. Moreover, PR dose-dependently induced lipid peroxidation and reduced superoxide dismutase activity. In contrast, PE induced a relatively mild hepatotoxicity. Intriguingly, the mixture of PR and PE did not reduce Liver Weight or increase serum aspartate transaminase activity. In addition, the mixture did not reduce the antioxidant enzyme activity as PR did. Thus, these results showed that PR induced prominent hepatotoxicity with subchronic exposure, and there is a potential antagonistic interaction between PR and PE on the oxidative damage in Liver of rats.
Jong-koo Kang - One of the best experts on this subject based on the ideXlab platform.
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Subchronic Oral Toxicity Study of Acanthopanax divaricatus var. albeofructus in Rats
Toxicological Research, 2017Co-Authors: Myoung Jun Kim, Mi Ju Lee, Yong-hoon Lee, Sun Hee Park, Duyeol Kim, Cheol Beom Park, Jin Seok Kang, Jong-koo KangAbstract:Acanthopanax divaricatus (Siebold & Zucc.) Seem. var. albeofructus (ADA), a traditional medical herb, has been used to treat arthritis and muscular injury, to strengthen muscle and bone, and to get vital energy. However, information regarding its toxicity is limited. ADA was administered by oral gavage to groups of rats at doses of 0 (control), 1,000, 1,500, 2,000, 2,500, and 3,000 mg/kg five times per week for 13 weeks. Mortality, clinical signs, body Weights, food consumption, hematology, serum chemistry, urinalysis, organ Weights, necropsy, histopathological finding, vaginal cytology, and sperm morphology were compared between control and ADA-treated groups. Salivation was intermittently observed in both sexes receiving 2,500 and 3,000 mg/kg directly after dosing. Absolute Liver Weights increased in females receiving 2,000, 2,500, and 3,000 mg/kg ADA ( P < 0.05, P < 0.01, and P < 0.01, respectively) and so did the relative Liver Weights ( P < 0.001). Salivation and increased Liver Weight were ADA-related changes but not considered to be adverse effects. Salivation was intermittent and transient, and the Liver Weight increase was minor and not accompanied by other changes such as hepatic morphological or functional alterations. The no-observed-adverse-effect-level was determined to be at least 3,000 mg/kg in both sexes of rats.
Yasutaka Kurata - One of the best experts on this subject based on the ideXlab platform.
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leukotrienes and cyclooxygenase products mediate anaphylactic venoconstriction in ovalbumin sensitized rat Livers
European Journal of Pharmacology, 2007Co-Authors: Toshishige Shibamoto, Hiromichi Takano, Wei Zhang, Yasutaka KurataAbstract:Hepatic anaphylactic venoconstriction is partly involved in anaphylactic hypotension. We determined the chemical mediators responsible for anaphylaxis-induced segmental venoconstriction in perfused Livers isolated from ovalbumin-sensitized rats. Livers were perfused portally and recirculatingly at constant flow with diluted blood. The portal venous pressure (Ppv), hepatic venous pressure (Phv), Liver Weight and hepatic oxygen consumption were continuously measured. The sinusoidal pressure was measured by the double occlusion pressure (Pdo), and was used to determine the pre-sinusoidal (Rpre) and post-sinusoidal (Rpost) resistances. After antigen injection, both Ppv and Pdo increased, resulting in 5.6- and 1.6-fold increases in Rpre and Rpost, respectively. Liver Weight showed a biphasic change of an initial decrease followed by an increase. Hepatic oxygen consumption significantly decreased after antigen. Anaphylaxis-induced increase in Rpre was most extensively inhibited by 38.6% by pretreatment with ONO-1078 (100 μM, a cysteinyl leukotriene receptor-1 antagonist), among all antagonists or inhibitors administrated individually including TCV-309 (20 μM), AA-2414 (10 μM), ketanserin (10 μM) and indomethacin (10 μM). Combined pretreatment with indomethacin and ONO-1078 exerted additive inhibitory effects and attenuated Rpre by 65.8%. However, TCV-309, a platelet activating factor (PAF) receptor antagonist, did not affect the anaphylactic response. In contrast, anaphylaxis-induced increase in Rpost was attenuated only by ONO-1078 combined pretreatment. The antigen-induced changes in Liver Weight and hepatic oxygen consumption were attenuated significantly when hepatic venoconstriction was attenuated. It is concluded that cysteinyl leukotrienes and cyclooxygenase products, but not PAF, are mainly involved in anaphylaxis-induced pre-sinusoidal constriction in isolated perfused rat Livers.
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hepatic venoconstriction is involved in anaphylactic hypotension in rats
American Journal of Physiology-heart and Circulatory Physiology, 2005Co-Authors: Toshishige Shibamoto, Zonghai Ruan, Hiromichi Takano, Yasutaka KurataAbstract:We determined the roles of Liver and splanchnic vascular bed in anaphylactic hypotension in anesthetized rats and the effects of anaphylaxis on hepatic vascular resistances and Liver Weight in isol...
A Bär - One of the best experts on this subject based on the ideXlab platform.
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Effect of D-tagatose on Liver Weight and glycogen content of rats.
Regulatory toxicology and pharmacology : RTP, 1999Co-Authors: A Bär, B A Lina, D M De Groot, B De Bie, M J AppelAbstract:D-tagatose is an incompletely absorbed ketohexose (stereoisomer of D-fructose) which has potential as an energy-reduced alternative sweetener. In an earlier 90-day toxicity study, rats fed diets with 10, 15 and 20% D-tagatose exhibited increased Liver Weights, but no histopathological alterations. To determine whether there might be any toxicological relevance to this effect, three studies were conducted in male, adult Sprague-Dawley rats. In the first study, four groups received Purina diet (group A), Purina diet with 20% D-tagatose (group B), SDS diet (group C), or SDS diet with 20% D-tagatose (group D). For groups A and B, the 28-day treatment period was followed by a 14-day recovery period (Purina diet). Food remained available to all animals until the time of sacrifice. Groups of 10 rats were killed on days 14 (groups A and B), 28 (groups A-D), and 42 (groups A and B). Body Weights, as well as Weights of wet and lyophilized Livers, were determined. The lyophilized Livers collected on day 28 from groups A and B were analyzed for protein, total lipid, glycogen, DNA, and residual moisture. By day 14, relative wet Liver Weights had increased by 23% in group B. On day 28, the increase was 38% in group B and 44% in group D. At the end of the recovery period, the increase had diminished to 14% in group B. On day 28, Liver glycogen content (in %) was significantly increased, and Liver protein, lipid, and DNA contents were significantly decreased in group B compared to group A. Total amounts per Liver of protein, total lipid, glycogen, and DNA were significantly increased. In the second study, four groups of 20 rats each received SDS diet with 0, 5, 10, and 20% D-tagatose for 29-31 days. The food was available until the time of sacrifice. At termination, plasma was obtained from 10 rats/group for clinicochemical analyses. Five rats/group were subjected to whole-body perfusion, followed by processing of Livers for qualitative and quantitative electron microscopic examination. Livers of 6 rats/group were analyzed for acyl-CoA oxidase and laurate 12-hydroxylase (cytochrome P450 4A1) activity, DNA synthesis (Ki-67 index), and number of nuclei per unit area of tissue. Liver Weights were significantly increased in linear relation to the D-tagatose intake. Plasma transaminases (but not glutamyl transferase and alkaline phosphatase) were increased in the high-dose group. Except for glycogen accumulation, no ultrastructural changes were seen on electron microscopic examination of Livers of the control and high-dose groups. Morphometric analysis confirmed the increase of glycogen and the absence of alterations of endoplasmatic reticulum, mitochondria, and Golgi apparatus. The Ki-67 index did not differ between the groups. A dose-related decrease of the number of nuclei per unit area signified some hepatocellular hypertrophy. Acyl-CoA oxidase and CYP4A1 activity were significantly increased in the mid- and high-dose groups, but these increases were small and not accompanied by electron-microscopic evidence of peroxisome proliferation. In the third study, four groups received SDS diet (groups A and C) or SDS diet with 5% D-tagatose (groups B and D). All animals were killed on day 28. Groups A and B were fasted for 24 h before sacrifice; groups C and D had food available until sacrifice. Liver Weights and Liver composition were measured as in Study 1. Relative wet and dry Liver Weights were increased in response to the treatment in rats killed under the fed condition, but not in rats killed under the fasted condition. The Livers of the treated rats (group D) had an increased glycogen content in comparison to the controls (group C). Taken together, these results demonstrate that D-tagatose at dietary levels of 5-20% increases Liver glycogen deposition and relative Liver Weights in nonfasting rats. In fasted rats the 5% dose level is the no-effect level. (ABSTRACT TRUNCATED)
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Effect of D-tagatose on Liver Weight and glycogen content of rats.
Regulatory Toxicology and Pharmacology, 1999Co-Authors: A Bär, B A Lina, D M De Groot, B De Bie, M J AppelAbstract:D-Tagatose is an incompletely absorbed ketohexose (stereoisomer of D-fructose) which has potential as an energy-reduced alternative sweetener. In an earlier 90-day toxicity study, rats fed diets with 10, 15 and 20% D-tagatose exhibited increased Liver Weights, but no histopathological alterations. To determine whether there might be any toxicological relevance to this effect, three studies were conducted in male, adult Sprague-Dawley rats. In the first study, four groups received Purina diet (group A), Purina diet with 20% D-tagatose (group B), SDS diet (group C), or SDS diet with 20% D-tagatose (group D). For groups A and B, the 28-day treatment period was followed by a 14-day recovery period (Purina diet). Food remained available to all animals until the time of sacrifice. Groups of 10 rats were killed on days 14 (groups A and B), 28 (groups A-D), and 42 (groups A and B). Body Weights, as well as Weights of wet and lyophilized Livers, were determined. The lyophilized Livers collected on day 28 from groups A and B were analyzed for protein, total lipid, glycogen, DNA, and residual moisture. By day 14, relative wet Liver Weights had increased by 23% in group B. On day 28, the increase was 38% in group B and 44% in group D. At the end of the recovery period, the increase had diminished to 14% in group B. On day 28, Liver glycogen content (in %) was significantly increased, and Liver protein, lipid, and DNA contents were significantly decreased in group B compared to group A. Total amounts per Liver of protein, total lipid, glycogen, and DNA were significantly increased. In the second study, four groups of 20 rats each received SDS diet with 0, 5, 10, and 20% D-tagatose for 29-31 days. The food was available until the time of sacrifice. At termination, plasma was obtained from 10 rats/group for clinicochemical analyses. Five rats/group were subjected to whole-body perfusion, followed by processing of Livers for qualitative and quantitative electron microscopic examination. Livers of 6 rats/group were analyzed for acyl-CoA oxidase and laurate 12-hydroxylase (cytochrome P450 4A1) activity, DNA synthesis (Ki-67 index), and number of nuclei per unit area of tissue. Liver Weights were significantly increased in linear relation to the D-tagatose intake. Plasma transaminases (but not glutamyl transferase and alkaline phosphatase) were increased in the high-dose group. Except for glycogen accumulation, no ultrastructural changes were seen on electron microscopic examination of Livers of the control and high-dose groups. Morphometric analysis confirmed the increase of glycogen and the absence of alterations of endoplasmatic reticulum, mitochondria, and Golgi apparatus. The Ki-67 index did not differ between the groups. A dose-related decrease of the number of nuclei per unit area signified some hepatocellular hypertrophy. Acyl-CoA oxidase and CYP4A1 activity were significantly increased in the mid- and high-dose groups, but these increases were small and not accompanied by electron-microscopic evidence of peroxisome proliferation. In the third study, four groups received SDS diet (groups A and C) or SDS diet with 5% D-tagatose (groups B and D). All animals were killed on day 28. Groups A and B were fasted for 24 h before sacrifice; groups C and D had food available until sacrifice. Liver Weights and Liver composition were measured as in Study 1. Relative wet and dry Liver Weights were increased in response to the treatment in rats killed under the fed condition, but not in rats killed under the fasted condition. The Livers of the treated rats (group D) had an increased glycogen content in comparison to the controls (group C). Taken together, these results demonstrate that D-tagatose at dietary levels of 5-20% increases Liver glycogen deposition and relative Liver Weights in nonfasting rats. In fasted rats the 5% dose level is the no-effect level. At the higher dose levels, the increased glycogen deposition induced minimal hypertrophy and some compensatory growth which reached completion before the end of the 28-day treatment period. It is concluded that the Liver enlargement seen in response to the consumption of D-tagatose is a physiological response to the treatment-induced increased glycogen deposition. No hepatocellular growth was seen at the 5% dietary level of D-tagatose (corresponding to an intake of 2.6-2.8 g/kg body wt), suggesting that the increase of Liver glycogen at this dose remained within normal limits. © 1999 Academic Press.
