Effect of 3,3′,4,4′-tetrachlorobiphenyl and 2,2′,4,4′,5,5′-hexachlorobiphenyl on the induction of hepatic lipid peroxidation and cytochrome P-450 associated enzyme activities in rats

Fadhel, Zaineb A.; Lu, Zijing; Robertson, Larry W.; Glauert, Howard P.

doi:10.1016/s0300-483x(02)00086-0

Cited by 47 publications

(37 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PCBs have been observed in many studies to induce oxidative stress. Several studies have shown that PCBs increase lipid peroxidation in the liver (Dogra et al 1988;Fadhel et al 2002;Kamohara et al 1984;Oda et al 1987;Pelissier et al 1990;Saito 1990;Shara and Stohs 1987;Yamamoto et al 1994). PCBs also can produce oxidative DMA damage, in the form of 8-hydroxydeoxyguanosine (Oakley et al 1996).…”

Section: Introductionmentioning

confidence: 99%

Role of oxidative stress in the promoting activities of PCBs

Glauert

Tharappel

et al. 2008

Environmental Toxicology and Pharmacology

Self Cite

View full text Add to dashboard Cite

PCBs are organic pollutants that persist and bioaccumulate in the environment. These chemicals induce and promote liver tumors in rodents. Previous studies have shown that they increase oxidative stress in the liver, including lipid peroxidation, oxidative DNA damage, and NF-κB activation. The objective of these studies was to determine if the promoting activities of PCBs could be inhibited by dietary antioxidants (vitamin E, selenium, or phytochemicals) or by knocking out the p50 subunit of NF-κB. In the antioxidant studies, female rats were first injected with DEN (150 mg/kg) and then administered 4 biweekly i.p. injections (300 μmol/kg/injection) of PCB-77, PCB-153, or vehicle; the number and volume of placental glutathione S-transferase (PGST)-positive foci were then quantified. Vitamin E did not influence the promoting activities of PCBs. Increasing dietary selenium above the recommended intake increased the number of foci induced but decreased their volume. Most of the phytochemicals examined (N-acetyl cysteine, β-carotene, resveratrol, EGCG) had no significant effect on the promoting activity of PCB-77. Ellagic acid increased and lycopene decreased the number of foci; ellagic acid, CoQ 10 , and curcumin decreased the volume of foci. In the NF-κB knockout study, male mice were first injected with DEN (90 mg/kg); controls not receiving DEN were also studied. Both p50 −/− and wild-type mice were then injected biweekly 20 times with PCB-153 (300 (μmol/kg). In DEN-treated and DEN + PCB-treated mice, the incidence of tumors was lower in the p50 −/− mice than in wild-type mice. In mice receiving PCB-153, the tumor incidence and tumor volume were higher. The volume of tumors that were positive for glutamine synthetase was increased in mice administered PCB-153. This study shows that the promotion of hepatocarcinogenesis by PCBs is largely unaffected by dietary antioxidants but is diminished when NF-κB activation is impaired by the absence of the p50 subunit.

show abstract

Section: Introductionmentioning

confidence: 99%

Role of oxidative stress in the promoting activities of PCBs

Glauert

Tharappel

et al. 2008

Environmental Toxicology and Pharmacology

Self Cite

View full text Add to dashboard Cite

show abstract

“…89 and others (90)(91)(92)]. Synergistic effects have been studied and have not been demonstrable (89,93). Nonetheless, there are a sufficient number of congener-specific studies that allow for the conclusion that the consistent finding in the epidemiologic literature is that individual congeners are not associated with breast cancer.…”

Section: Polychlorinated Biphenylsmentioning

confidence: 94%

Understanding Population and Individual Risk Assessment: The Case of Polychlorinated Biphenyls

Shields

2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

View full text Add to dashboard Cite

Decisions about how to improve or protect the public health can be, and sometimes necessarily are, made on imprecise science. The regulation of potential human carcinogens in the environment entails a population-risk assessment process intended to reduce risks to less than one additional cancer in 100,000 or 1,000,000 persons. These risk assessment processes, however, may be miscommunicated or misinterpreted in the context of individual cancer risks by scientists, regulators, the lay media, and the public. This commentary will review methods for establishing a causal relationship between carcinogen exposures and cancer risk. It will use the case of polychlorinated biphenyls (PCB) as an example of how to place scientific data into the context of human exposure and cancer risk. PCBs are widespread environmental contaminants and most people have detectable levels of PCBs in their bodies. The primary source for exposure in the general population is through the diet. PCBs are carcinogens in experimental animal models, but how this information can be extrapolated to human risk remains uncertain. PCB experimental studies provide data that are used to regulate and control human exposure, although the epidemiologic evidence fails to establish PCBs as human carcinogens. Thus, what is used for populationrisk assessment may not be appropriate for individual-risk assessment or concluding that a causal relationship exists between PCB exposure and cancer risk. The hazards from a carcinogen designated by regulatory and review agencies as a ''probable'' human carcinogen is often misunderstood out of context about the magnitude of the risk and in what settings. How scientists communicate their results in scientific articles can strongly influence how others interpret their data. Misunderstandings from both the use of regulatory and review-agency opinions and the conclusions espoused by scientists occur in the media, among private physicians counseling their patients about cancer risk, and in the legal settings where plaintiffs seek compensation for exposure and alleged harm (or future harm). This can lead to false conclusions about what caused a cancer in a specific patient, undue anxiety about future cancer risk, inappropriate cancer screening, and attendant increased morbidity due to increased uses of the medical system and complication rates from medical procedures. The communication of research findings by scientists must be presented with caution, resisting the temptation to extrapolate, inappropriately, research data to the general population. (Cancer Epidemiol Biomarkers Prev 2006;15(5):830 -9)

show abstract

“…26) Additionally, xenobiotics induce hepatic lipid peroxidation. 27) It has been hypothesized that a central cause of xenobiotic-induced hepatotoxicity is excessive lipid peroxidation. Hepatic gene expression of Cyp2b1/2b2 was induced by chloretone (Fig.…”

Section: Discussionmentioning

confidence: 99%