Toxicity of trans-nonachlor to Sprague–Dawley rats in a 90-day feeding study

Bondy, Genevieve S.; Curran, Ivan; Doucet, Josée; Armstrong, Cheryl; Coady, Laurie; Hierlihy, L.; Fernie, S.; Robertson, Patrick; Barker, Michael

doi:10.1016/j.fct.2004.02.014

Cited by 34 publications

(23 citation statements)

References 32 publications

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“…OxC has previously been linked with a range of chemically induced stress responses in a selection of species (Bondy et al 2004; Kunisue et al 2007; Murvoll et al 2007). Kunisue et al (2007) and Bondy et al (2004) pointed out the high persistency of oxychlordane.…”

Section: Discussionmentioning

confidence: 99%

Measuring environmental stress in East Greenland polar bears, 1892–1927 and 1988–2009: What does hair cortisol tell us?

Bechshøft

Rigét

Sonne

et al. 2012

Environment International

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Hair sampled from 96 East Greenland polar bears (Ursus maritimus) over the periods 1892–1927 and 1988–2009 was analyzed for cortisol as a proxy to investigate temporal patterns of environmental stress. Cortisol concentration was independent of sex and age, and was found at significantly higher (p < 0.001) concentrations in historical hair samples (1892–1927; n = 8) relative to recent ones (1988–2009; n = 88). In addition, there was a linear time trend in cortisol concentration of the recent samples (p < 0.01), with an annual decrease of 2.7 %. The recent hair samples were also analyzed for major bioaccumulative, persistent organic pollutants (POPs). There were no obvious POP related time trends or correlations between hair cortisol and hair POP concentrations. Thus, polar bear hair appears to be a relatively poor indicator of the animal’s general POP load in adipose tissue. However, further investigations are warranted to explore the reasons for the temporal decrease found in the bears’ hair cortisol levels.

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Section: Discussionmentioning

confidence: 99%

Measuring environmental stress in East Greenland polar bears, 1892–1927 and 1988–2009: What does hair cortisol tell us?

Bechshøft

Rigét

Sonne

et al. 2012

Environment International

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“…This extraction methodology has been used in our laboratory for many years to evaluate POPs in various matrices (Bondy et al 2003, 2004). The GC-MS method allows for the concurrent analysis and quantification of several OC pesticides and PCB and PBDE congeners, facilitating extensive data acquisition from small specimens.…”

Section: Methodsmentioning

confidence: 99%

Persistent Organic Pollutant Residues in Human Fetal Liver and Placenta from Greater Montreal, Quebec: A Longitudinal Study from 1998 through 2006

Doucet

Tague

Arnold

et al. 2009

Environ Health Perspect

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BackgroundThere is general concern that persistent organic pollutants (POPs) found in the environment, wildlife, food, water, house dust, human tissues, and fluids may alter normal human physiologic activities (e.g., fetal development, immune and endocrine systems). Although the levels of some POPs [polychlorinated biphenyls (PCBs) and organochlorine pesticides (OCs)] in these matrices have decreased after their ban, others [polybrominated diphenyl ethers (PBDEs)] have increased in recent years.ObjectiveTo determine the longitudinal trend of specific POPs in human fetal tissues for risk assessment purposes.MethodsWe analyzed early to mid-gestation fetal liver (n = 52) and placental (n = 60) tissues, obtained after elective abortions during 1998–2006, for selected PBDEs, PCBs, and OCs using gas chromatography–mass spectroscopy.ResultsTotal PBDEs in fetal liver increased over time (mean ± SE: 1998, 284.4 ± 229.8 ng/g lipid; 2006, 1,607.7 ± 605.9; p < 0.03), whereas placental levels were generally lower, with no clear trend. Low levels of PCBs and OCs varied yearly, with no evident trend. The major analytes in 1998 were OCs (liver, 49%; placenta, 71%), whereas the major analytes in 2006 were PBDEs (liver, 89%; placenta, 98%). The 1998–2006 tissue PBDE congener profile is similar to that of DE-71, a commercial primarily pentabrominated diphenyl ether mixture manufactured in North America.ConclusionsAlthough commercial production of penta- and octa-brominated diphenyl ethers in North America was halted in 2004, their concentrations in fetal liver and placenta are now greater than the tissue burdens for the analyzed OCs and PCBs. Our findings also demonstrate that PBDEs accumulate within the fetal compartment at a very early stage in gestation.

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“…[1920] Similarly, trans-nonachlor (an analog of CLD) has been reported to increase hepatic lipid peroxidation via CYP induction, resulting in the release of activated toxic oxygen species. [13] Other chlorinated hydrocarbons such as polychlorinated biphenyls that are inducers of CYP enzymes have also been linked to the production of lipid peroxidation in the liver. [21]…”

Section: Resultsmentioning

confidence: 99%

“…[12] Induction of hepatic xenobiotic-metabolizing enzymes by chlorinated hydrocarbons including CLD has been linked to multiple effects on endocrine organs such as thyroid and adrenal gland. [13] This prompted us to use CLD as a typical inducer of hepatic CYP enzymes to examine if CLD-inducible CYPs can potentiate the hepatic toxicity of CS 2 in the rats exposed to CS 2 .…”

Section: Introductionmentioning

confidence: 99%

Potentiation of the hepatic toxicity of carbon disulfide by chlordane

Dalvi

Billups

2013

Toxicol Int

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Objectives:In this study, we investigated whether cytochrome P450s (CYPs) induced by a typical chlorinated hydrocarbon insecticide chlordane (CLD) potentiate hepatic toxicity of carbon disulfide (CS2).Materials and Methods:Male Sprague-Dawley rats were treated with CLD (25 mg/kg, intraperitoneally (i.p.)) daily for 4 days, and 24 h after the final injection the rats were treated with CS2 (380 mg/kg, i.p.) in corn oil; while controls received the vehicle alone. The rats were then sacrificed at 3, 6, and 24 h following the CS2 treatment.Results:It was found that at 3 h post-treatment, total hepatic glutathione (GSH) decreased modestly, but lipid peroxidation increased markedly, while all CLD-inducible CYPs (1A1, 2B1, 2E1, and 3A2) were inhibited by CS2 variably but significantly. On the other hand, samples taken at 24 h following the CS2 treatment showed a significant increase in relative liver weights, hepatic GSH and lipid peroxidation, microsomal reactive oxygen species (ROS), and serum alanine transaminase (ALT) level. Activity of the CYPs was also increased, but remained significantly depressed, especially that of CYP2B1. Livers removed at 3 and 6 h after CS2 treatment showed subtle to distinct apoptotic changes, while a severe lesion of hydropic degeneration of the centrilobular cells with apoptosis was microscopically distinguishable in samples taken at 24 h.Conclusions:These results suggest that the metabolism of CS2 by CLD-induced CYPs and the generation of lipid peroxides may have in concert contributed to the distinct hepatocellular damage.

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Toxicity of trans-nonachlor to Sprague–Dawley rats in a 90-day feeding study

Cited by 34 publications

References 32 publications

Measuring environmental stress in East Greenland polar bears, 1892–1927 and 1988–2009: What does hair cortisol tell us?

Measuring environmental stress in East Greenland polar bears, 1892–1927 and 1988–2009: What does hair cortisol tell us?

Persistent Organic Pollutant Residues in Human Fetal Liver and Placenta from Greater Montreal, Quebec: A Longitudinal Study from 1998 through 2006

Potentiation of the hepatic toxicity of carbon disulfide by chlordane

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