2,3,7,8-Tetrachlorodibenzo-p-dioxin affects retinol esterification in rat hepatic stellate cells and kidney

Nilsson, Charlotte B.; Hanberg, Annika; Trossvik, Christina; Håkansson, Helen

doi:10.1016/1382-6689(96)00023-3

Cited by 37 publications

(12 citation statements)

References 29 publications

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“…The suppressed LRAT activity in TCDD-exposed rats is considered to be most likely related to the inhibited vitamin A storage in stellate cells [26]. Some studies demonstrated that in whole rat liver tissue, LRAT activity was not decreased by TCDD [26] or that rat hepatic LRAT activity was slightly increased by TCDD [19]. However, in our study, TCDD had no significant effect on LRAT mRNA in whole mouse liver.…”

Section: Discussioncontrasting

confidence: 57%

“…LRAT is considered an important enzyme, which esterifies cytosolic retinol [27] and is regulated by dietary vitamin A or RA [28]. The suppressed LRAT activity in TCDD-exposed rats is considered to be most likely related to the inhibited vitamin A storage in stellate cells [26]. Some studies demonstrated that in whole rat liver tissue, LRAT activity was not decreased by TCDD [26] or that rat hepatic LRAT activity was slightly increased by TCDD [19].…”

Section: Discussionmentioning

confidence: 99%

“…Suitable storage of vitamin A is required for maintenance of vitamin A homeostasis, but TCDD decreases the hepatic vitamin A storage in animals, especially in the hepatic stellate cells of rats [26]. Therefore, TCDD may inhibit the vitamin A net accumulation in liver by interference with the dynamic balance between esterification of retinol and hydrolysis of stored retinyl ethers.…”

Section: Discussionmentioning

confidence: 99%

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Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on vitamin A metabolism in mice

Yang

Huang

Liu

et al. 2005

J. Biochem. Mol. Toxicol.

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This study aimed to clarify the effects of single and repeated administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the activities or expression of some metabolic enzymes of retinoids and the influence of supplemental vitamin A on changed vitamin A homeostasis by TCDD. In Experiment I, the mice were given a single oral dose of 40 mug TCDD/kg body weight, with or without continuous administration of 2,500 IU vitamin A/kg body weight/day, and were killed on day 1, 3, 7, 14, and 28. In Experiment II, the mice were daily given 0.1 microg TCDD/kg body weight, with or without supplemental 2,000 IU vitamin A/kg body weight, and were killed on day 14, 28, and 42. In both experiments, TCDD significantly decreased the hepatic all-trans-retinol level and increased the hepatic all-trans-retinoic acid (RA) content, increased the mRNA and enzymatic activities of retinal oxidase. In TCDD + vitamin A mice, the all-trans retinol content was significantly higher, and the retinal oxidase mRNA was significantly lower on day 3 or 7 in Experiment I and on day 14 in Experiment II, compared to TCDD-treated mice. The induction of the retinal oxidase may contribute to the decrease in hepatic all-trans-retinol level and the increase in hepatic all-trans-RA caused by TCDD. Supplemental vitamin A might decelerate the effect of TCDD on retinal oxidase mRNA.

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Section: Discussioncontrasting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on vitamin A metabolism in mice

Yang

Huang

Liu

et al. 2005

J. Biochem. Mol. Toxicol.

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“…One explanation may lie in the decreased LRAT and ARAT activities, two enzymes involved in the conversion of retinol into retinyl esters in hepatic stellate cells (D'Ambrosio et al, 2011), and thus in the hepatic storage of vitamin A. Indeed, it has been shown that the treatment of rats with TCDD induced a decreased activity of LRAT and ARAT (Nilsson et al, 1996). As coplanar PCBs are agonists of the AhR in a similar way to TCDD and the impact of TCDD on vitamin A metabolism occurs entirely via AhR (Nová k et al, 2008), coplanar PCBs, such as CB-105 and -118, may also be able to induce comparable enzyme inhibition.…”

Section: Relationships Between Pcbs Ho-pcbs and Vitamin Amentioning

confidence: 99%

“…The activity of enzymes that esterify retinol and hydrolyse retinyl esters such as retinyl ester hydrolase (REH), acyl-CoA:retinol acyltransferase (ARAT) and lecithin:retinol acyltransferase (LRAT) were also shown to be modulated by PCBs and TCDD in fish and laboratory animals ( Fig. 1, points 3, 4 and 8) (Chen et al, 1992;Nilsson et al, 1996;Ndayibagira and Spear, 1999;Nilsson et al, 2000). In addition, some hydroxylated PCB metabolites (HO-PCBs) can interact with transthyretin (TTR), as reported in vivo and in vitro in humans and rats.…”

Section: Introductionmentioning

confidence: 99%

Effects of polychlorobiphenyls, polybromodiphenylethers, organochlorine pesticides and their metabolites on vitamin A status in lactating grey seals

Berghe

Weijs

Habran

et al. 2013

Environmental Research

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a b s t r a c tPolychlorobiphenyls (PCBs), polybromodiphenylethers (PBDEs) and organochlorine pesticides (OCPs), such as dichlorodiphenyltrichloroethane (DDT) and hexachlorobenzene (HCB), are considered as endocrine disruptors in laboratory and wild animals. This study investigated whether these compounds and their hydroxylated metabolites (HO-PCBs and HO-PBDEs) may affect the homoeostasis of vitamin A, a dietary hormone, in the blubber and serum of twenty lactating grey seals sampled at early and late lactation on the Isle of May, Scotland. The effect of naturally produced compounds such as the methoxylated (MeO)-PBDEs was also examined. Vitamin A levels in inner blubber (37 7 9 mg/g wet weight (ww) and 92 7 32 mg/g ww at early and late lactation, respectively) and serum (408 7 143 and 390 7 98 ng/ml at early and late lactation, respectively) appeared to be positively related to SPCBs, SPBDEs and several individual PCB and PBDE congeners in inner blubber and serum. These findings may suggest enhanced mobilisation of hepatic retinoid stores and redistribution in the blubber, a storage site for vitamin A in marine mammals. We have also reported that serum concentrations of SHO-PCBs and 4-OH-CB107 tended to increase with circulating vitamin A levels. Although the direction of the relationships may sometimes differ from those reported in the literature, our results are in agreement with previous findings highlighting a disruption of vitamin A homoeostasis in the blubber and bloodstream following exposure to environmental pollutants. The fact that vitamin A and PCBs appeared to share common mechanisms of mobilisation and transfer during lactation in grey seals (Debier et al., 2004;Vanden Berghe et al., 2010) may also play a role in the different relationships observed between vitamin A and lipophilic pollutants.

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Chronic and reproductive toxicity of a mixture of 15 methylsulfonyl‐polychlorinated biphenyls and 3‐methylsulfonyl‐2,2‐bis‐(4‐chlorophenyl)‐1,1‐dichloroethene in mink (Mustela vison)

Lund

Örberg

Bergman

et al. 1999

Enviro Toxic and Chemistry

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Abstract-A synthetic mixture of 16 aryl methyl sulfones was given in the feed to female mink for one year (three times a week, resulting in a mean daily exposure of 0.1 mg/mink). The mink were mated after 9 months of exposure and the reproductive outcome was studied. The dams and kits were examined for biochemical and toxic effects. The litter size was significantly increased (50%) in the exposed group, and the mean birth weight was 20% lower than that of the controls. Kit survival was 47% by 2 weeks after birth in the exposed group, as compared to 73% in the control group. Both adults and kits had induced (5-to 11-fold) hepatic activities of pentoxyresorufin-O-dealkylase. In livers from the dams, catabolism of progesterone in vitro was increased almost twofold. Decreased thyroid hormone concentrations (total triiodothyronine and total thyroxine, 30-35% of control values) in plasma were observed in the adults. The bioaccumulation factor for the mixture of 3-and 4-methylsulfonyl-polychlorinated biphenyls (PCBs) was 2.1 (muscle vs feed concentration). The 3-methylsulfonyl-PCBs accumulated 2-to 65-fold in liver relative to muscle and lung. At the cessation of the exposure period, the total concentrations of aryl methyl sulfones in the dams and their 5-weekold kits were 18 Ϯ 2 and 21 Ϯ 3 g/g, respectively (lipid weight, muscle), demonstrating significant transport from dams to kits and accumulation in the kits.

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2,3,7,8-Tetrachlorodibenzo-p-dioxin affects retinol esterification in rat hepatic stellate cells and kidney

Cited by 37 publications

References 29 publications

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on vitamin A metabolism in mice

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on vitamin A metabolism in mice

Effects of polychlorobiphenyls, polybromodiphenylethers, organochlorine pesticides and their metabolites on vitamin A status in lactating grey seals

Chronic and reproductive toxicity of a mixture of 15 methylsulfonyl‐polychlorinated biphenyls and 3‐methylsulfonyl‐2,2‐bis‐(4‐chlorophenyl)‐1,1‐dichloroethene in mink (Mustela vison)

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