It is known that the LEC (Long-Evans Cinnamon) rat, an inbred strain of a mutant rat isolated from Long-Evans rats, has spontaneously developed acute hepatitis accompanied with severe jaundice about 4 months after birth, and that the copper metabolism in the LEC rat is abnormal, its clinical signs resemble W ilson's disease. The green-pigmented incisors in LEC rat erupted 3 weeks after hereditary hepatitis, and the pigmentation might be caused by bilirubin from histopathological analysis was reported. In this study, to elucidate the cause of pigmentation, the copper and bilirubin concentration in the pigmented teeth was examined using energy dispersive x-ray analysis (EDX), atomic absorption analysis, and determination of light absorption analysis. In the pigmented area, the peak of copper was not recognized with point analysis using EDX. As a result of atomic absorption copper analysis, LEC rat pigmented teeth contained 6.833±2.353 (ppm) and normal LEA (Long-Evans Agouti) rat teeth contained 2.884±1.183 (ppm). Copper concentration of both teeth were minimal. Bilirubin analysis indicated that in LEA normal teeth bilirubin was not detected but that in LEC pigmentedteeth bilirubin was detected as in LEA artificial pigmented teeth caused by bile duct ligature and bilirubin administration. These results indicated that the pigmentation in LEC rat was caused by bilirubin. Thus LEC rat seems to be a very useful animal model for analysis of the pigmented teeth caused by bilirubin.
