Results of a two-year chronic toxicity and oncogenicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats
References (9)
- et al.
Morphological change in monkeys consuming a diet containing five hundred parts per trillion of 2,3,7,8 tetrachlorodibenzo-p-dioxin
Food Cosmet. Toxicol.
(1977) - et al.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCCD): Results of a 13-week oral toxicity study in rats
Toxicol. Appl. Pharmacol.
(1976) - et al.
Toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rhesus monkeys (Macaca mulatta) following a single oral dose
Toxicol. Appl. Pharmacol.
(1978) - et al.
Increased incidence of neoplasms in rats exposed to low levels of 2,3,7,8-tetrachlorodibenzo-o-dioxin
Chemosphere
(1977)
Cited by (25)
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) alters hepatic polyunsaturated fatty acid metabolism and eicosanoid biosynthesis in female Sprague-Dawley rats
2020, Toxicology and Applied PharmacologyCitation Excerpt :Integration of differential gene expression with complementary untargeted metabolomics demonstrated that PUFA metabolism and eicosanoid biosynthesis were disrupted by TCDD. These changes increased inflammatory lipid mediators which may be contributing to increased inflammation in chronically exposed rats (Kociba et al., 1978; NTP, 1994; Walker et al., 2006). Based on BMD values for differential gene expression with correlative changes in metabolites, the cytochrome P450 hydroxylation/epoxidation pathway and the lipoxygenase pathways were more sensitive to TCDD than the cyclooxygenase pathway.
Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on spontaneous movement of human neuroblastoma cells
2020, Science of the Total EnvironmentCitation Excerpt :Epidemiological study on the long-term health impacts of TCDD exposure showed that the incidence of all cancers was increased in the population exposed to TCDD in Seveso, Italy (Bertazzi et al., 1989). Moreover, after a two-year chronic exposure to TCDD at a relative low concentration (0.01 μg/kg/day, equivalent to 210 ppt), the rats encountered an increased risk of various squamous cell carcinomas and hepatocellular carcinoma (Kociba et al., 1978). In addition to the increased risk of cancer occurrence, a retrospective cohort study in the United States indicated that workers exposed to TCDD had an increased mortality from various cancers, especially those with the longest occupational exposure to TCDD (Fingerhut et al., 1991).
The impact of maternally derived dioxins on embryonic development and hepatic AHR signaling in a long-lived apex predator
2019, ChemosphereCitation Excerpt :Despite these possible effects, very little is known regarding toxicokinetics of these contaminants in the alligator, including inducibility of the AHR-responsive gene battery that mediates toxicity and clearance (but see Ertl and Winston, 1998; Ertl et al., 1998; Ertl et al., 1999a,b). Nonetheless, dioxins are capable of eliciting adverse effects at low doses during development (Sato et al., 2008; Ohsako et al., 2001; Haijima et al., 2010; Faqi et al., 1998) and in adulthood following chronic exposure (Brulport et al., 2017; Kociba et al., 1978), suggesting that dioxin and related contaminants might pose a substantive threat in exposed alligator populations. Given the persistent nature of these contaminants and the important ecological role for crocodilians (Mazzotti et al., 2009), we believe that a broader investigation of the prevalence and effects of dioxin in wild populations is warranted.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) effects on hepatic microsomal cytochrome P-448-mediated enzyme activities
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