Studies on the Mechanism of Toxicity of DDT and Polychlorinated Biphenyls: Disruption of Osmoregulation in Marine Fish

In 1970 studies were initiated at the Mount Desert Island Biological Laboratory to explore mechanisms of toxicity underlying the high sensitivity of bony fish, teleosts, to organochlorine pollutants. The starting point was several reports that DDT [1 ,1, 1-trichloro-2, 2-bis (p-chlorophenyl) ethane] inhibited Na, K-ATPase (Na+, K+-activated adenosine triphosphatase), as well as the knowledge that this enzyme appears to play a central role in osmoregulation by marine teleosts. In the face of a desiccative environment, these fish maintain body fluid hypotonicity (Fig. 1) by drinking sea water, absorbing water coupled with salts across the intestinal epithelium, and eventually secreting the NaCl across the gill epithelium while retaining the free water. The primary driving mechanism in both intestine and gill is the Na pump with which Na, K-ATPase appears to be intimately involved. For fuller discussion, see (2) and (3). After demonstrating that DDT did, in fact, inhibit Na, K-ATPase activity in homogenates of intestinal mucosa and gill filaments from several marine teleosts (2), attention was focused on the sea water-adapted eel (Anguilla rostrata), in which osmoregulation has been well investigated. This eel can also adapt to fresh water and can be used for future DDT studies.