Mink (Mustela vison) exposed to 2,3,7,8,-tetrachlorodibenzodioxin (TCDD) and other TCDD-like compounds, such as 3,3',4,4',5-pentachlorobiphenyl (PCB 126), develop an invasive jaw lesion characterized histologically as mandibular and maxillary squamous cell proliferation. Jaw lesions have been reported in wild mink residing in environments contaminated with TCDD-like chemicals and there is evidence suggesting jaw-related lesions in other wildlife species exposed to TCDD-like chemicals. To date, no studies have been published addressing the etiology of this lesion, but the aryl hydrocarbon receptor (AhR) is assumed to be involved because of the lesion's induction by TCDD-like chemicals. To further examine the development of the lesion, two studies were conducted. The first study was a timeline study of the development of the lesion over a period of 28 days in mink exposed to 30 μg PCB 126/kg feed. In the second study, resveratrol, an AhR antagonist, was administered (6 daily gavage doses of 50 mg resveratrol/kg bw) to mink dosed with PCB 126 (a single IP injection of 30 μg PCB 126/kg bw following the last dose of resveratrol) to determine if it could prevent or reduce the development of the lesion. Resveratrol had no apparent effect on the incidence or severity of the PCB 126-induced effects
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