Correlation of 2,3,7,8-Tetrachlorodibenzo-p-dioxin Induction of Cytochrome P4501A in Vascular Endothelium with Toxicity in Early Life Stages of Lake Trout

Guiney, Patrick D.; Smolowitz, Roxanna; Peterson, Richard E.; Stegeman, John J.

doi:10.1006/taap.1996.8051

Cited by 143 publications

(99 citation statements)

References 43 publications

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“…Fundulus embryos exposed to TCDD had defects similar to other fish embryos Cantrell et al 1996Cantrell et al , 1998Guiney et al, 1997;Hornung et al, 1999) including hemorrhaging, edema, loss of blood flow, and stunted development. Our injection data of the toxicity of TCDD indicates that Fundulus embryos (LD 50 : 250 pg/g embryo) were more sensitive than medaka embryos (LC 50egg : 1250 pg/g egg) and zebrafish embryos (LC 50egg : 2500 pg/g egg) and less sensitive than lake trout embryos (LC 50egg : 50-100 pg/g egg) (Elonen et al, 1998).…”

Section: Discussionmentioning

confidence: 84%

“…Furthermore, TCDD-induced vascular cell death was correlated with embryotoxicity and co-localized with CYP1A expression in the vasculature of medaka, and sublethal doses of TCDD increased cell death in digestive and gill tissues (Cantrell et al, 1998). In TCDD-exposed trout embryos, endothelial CYP1A expression and sac fry mortality occurred with similar dose -response relationships (Guiney, et al, 1997).…”

Section: Introductionmentioning

confidence: 94%

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2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos

et al. 2001

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Section: Discussionmentioning

confidence: 84%

Section: Introductionmentioning

confidence: 94%

2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos

et al. 2001

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“…Fish embryos are highly sensitive to TCDD and show circulation failure, edema, craniofacial malformation and death [12]. It has been reported that in fish embryos CYP1A can be induced by TCDD and that there is a correlation of that induction with TCDD-induced toxicity [2,5,10]. However, detailed localization of CYP1A mRNA and protein expressions, especially in their relationship, remains to be determined in early fish embryos.…”

mentioning

confidence: 99%

cDNA Cloning and Expressions of Cytochrome P450 1A in Zebrafish Embryos.

Yamazaki

Teraoka

Wang

et al. 2002

The Journal of Veterinary Medical Science

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ABSTRACT. Cytochrome P450 1A (CYP1A) is well known for being induced by aromatic hydrocarbons, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). We determined the complete cDNA sequence of a CYP1A open reading frame with both 5'-and 3'-ends in zebrafish (zfCYP1A), a useful model for environmental toxicology. zfCYP1A shows high percentage identity with CYP1As of mammals, domestic fowl and xenopus (51.9-60.4%), as well as the other fish species (63.8-89.2%). As revealed by in situ hybridization and immunohistochemistry, zfCYP1A was scarcely detected in control embryos but was markedly induced by TCDD especially in heart, vascular endothelial cells, intestinal epithelium, pronephros and outer integument in both prehatched and hatched embryos. These e xpression patterns are consistent with possible involvement of zfCYP1A in TCDD-induced toxicities. KEY WORDS: CYP1A, TCDD, zebrafish.

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“…OCPs can induce early-lifestage mortality through three mechanisms: 1) direct toxicity to developing embryos, 2) altered maternal vitellogenesis and oogenesis leading to changes in egg composition, and/or 3) immunosuppression. Direct toxicity of chlorinated organics has been extensively characterized after exposure of early-life stages of fish to aryl hydrocarbon receptor (AhR) agonists (mostly dioxins and polychlorinated biphenyls [PCBs], but also OCPs) (Smith and Cole, 1973;Monod, 1985;Guiney et al, 1997;Henry et al, 1997). In these studies, mortality was associated with yolk sac and pericardial edema, craniofacial alterations, and severe and generalized hemovascular damage.…”

Section: Relationship Between Ocps and Abnormalitiesmentioning

confidence: 99%

Necropsy Findings in American Alligator Late-Stage Embryos and Hatchlings From Northcentral Florida Lakes Contaminated With Organochlorine Pesticides

Sepúlveda

Piero

Wiebe³

et al. 2006

Journal of Wildlife Diseases

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ABSTRACT:Increased American alligator (Alligator mississippiensis) embryo and neonatal mortality has been reported from several northcentral Florida lakes contaminated with old-use organochlorine pesticides (OCPs). However, a clear relationship among these contaminants and egg viability has not been established, suggesting the involvement of additional factors in these mortalities. Thus, the main objective of this study was to determine the ultimate cause of mortality of American alligator late-stage embryos and hatchlings through the conduction of detailed pathological examinations, and to evaluate better the role of OCPs in these mortalities. Between 2000 and 2001, 236 dead alligators were necropsied at or near hatching (after ,65 days of artificial incubation and up to 1 mo of age posthatch). Dead animals were collected from 18 clutches ranging in viability from 0% to 95%. Total OCP concentrations in yolk ranged from ,100 to 52,000 mg/kg, wet weight. The most common gross findings were generalized edema (34%) and organ hyperemia (29%), followed by severe emaciation (14%) and gross deformities (3%). Histopathologic examination revealed lesions in 35% of the animals, with over half of the cases being pneumonia, pulmonary edema, and atelectasis. Within and across clutches, dead embryos and hatchlings compared with their live cohorts were significantly smaller and lighter. Although alterations in growth and development were not related to yolk OCPs, there was an increase in prevalence of histologic lesions in clutches with high OCPs. Overall, these results indicate that general growth retardation and respiratory abnormalities were a major contributing factor in observed mortalities and that contaminants may increase the susceptibility of animals to developing certain pathologic conditions.

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Correlation of 2,3,7,8-Tetrachlorodibenzo-p-dioxin Induction of Cytochrome P4501A in Vascular Endothelium with Toxicity in Early Life Stages of Lake Trout

Cited by 143 publications

References 43 publications

2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos

2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos

cDNA Cloning and Expressions of Cytochrome P450 1A in Zebrafish Embryos.

Necropsy Findings in American Alligator Late-Stage Embryos and Hatchlings From Northcentral Florida Lakes Contaminated With Organochlorine Pesticides

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