Among the environmental chemicals that may be able to disrupt the endocrine systems of animals and humans are polychlorinated biphenyls (PCBs), a chemical class of considerable concern. PCB consists of two six-carbon rings linked by a single carbon bond, and theoretically, 209 congeners can form, depending on the number of chlorines and their location on the biphenyl rings. Furthermore, 3,3’,4,4’,5-pentachlorobiphenyl (PCB126) exposure also increases nitric oxide production and nuclear factor kappa-light-chain-enhancer of activated B cells binding activity in chondrocytes, thus contributing as an initiator of chondrocyte apoptosis and resulting in thymic atrophy and immunosuppression. This study identified whether cardiac and immune abnormalities from PCB126 were caused by the Kv1.3 and Kv1.5 channels. PCB126 did not affect either the steady-state current or peak current of the Kv1.3 and Kv1.5 channels. However, PCB126 right-shifted the steady-state activation curves of human Kv1.3 channels. These results suggest that PCBs can affect the heart in a way that does not block voltage-dependent potassium channels including Kv1.3 and Kv1.5 directly.

This study was conducted to examine the effect of 3,3',4,4',5-pentachlorobiphenyl (PCB 126) on morphological changes in the developing rat testis. PCB 126 (0.2㎎/㎏/week) in corn oil was weekly i.p. injected into rats from 1 to 11 weeks old. The total body weights and testicular weights were measured at 3, 6, 9 and 12 weeks, respectively. The morphological changes in the rat testes were then analyzed by light microscopy (LM) and transmission electron microscopy (TEM). The results demonstrated that PCB 126 treatment caused significant change in the ratio of testicular weight/body weight at 9 week. The treatment of PCB increased the number of pregonium cells at 3 week and it decreased spermatogenesis of the seminiferous tubules at 6 week. The results of this study suggest that PCB 126 can damage the male reproductive organ of the growing rat and that it might be associated with retardation of development of the testis.