The degree of PCB chlorination determines whether the rise in urinary homovanillic acid production in rats is peripheral or central in origin.

Commercial mixtures of polychlorinated biphenyls (PCBs, Aroclor 1016, 1254, and 1260) differing in their degree of chlorination and their accumulation in the brain were employed along with a peripheral monoamine oxidase inhibitor, debrisoquin sulfate (Declinax, DS) to determine whether the rise in urinary homovanillic acid (UHVA) following exposure to these PCBs is derived from the peripheral or central nervous system. Rats were gavaged with either corn oil or corn oil containing Aroclor 1016 or a mixture of Aroclors 1254 and 1260 and 24-hr UHVA production was determined by high-performance liquid chromatography with electrochemical detection. All animals also received ip injections of DS to inhibit peripheral production of HVA. Analysis of variance indicated that, following DS treatment, 24-hr UHVA production remained significantly elevated in the Aroclor 1254/1260-exposed animals; while no significant differences between Aroclor 1016-exposed animals and controls were noted. The rise in UHVA in the Aroclor 1254/1260 group involves HVA of central origin whereas the rise in the Aroclor 1016-treated animals is only peripheral. Thus, PCBs that differ in their degree of chlorination alter dopaminergic functions in anatomically different locations.