|Straus, David - Dave|
Submitted to: Australasian Society Of Ecotoxicology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 4/24/1998
Publication Date: N/A
Citation: STRAUS, D.L., STUTHRIDGE, T., ANDERSON, S.M., GIFFORD, J.S. ACUTE TOXICITY OF DEHYDROABIETIC ACID TO RAINBOW TROUT: MANIPULATION OF ENZYME. AUSTRALASIAN SOCIETY OF ECOTOXICOLOGY. 1998. v.3. p.131-197. Interpretive Summary: Resin acids are the most deadly chemicals to fish in the waste waters of pulp mills; there is a specific one (dehydroabietic acid) that is present in large amounts and remains in the environment longer. The acute toxicity of this resin acid has been determined in rainbow trout, but we wanted to see if certain chemicals could make it more toxic by controlling the enzymes that make it toxic. We tested 2 chemicals and found that piperonyl butoxide (a commonly found in insect repellant) made the resin acid more toxic; the other chemical didn't cause an effect. Further tests showed that piperonyl butoxide makes a certain group of enzymes of the fish work harder to make the resin acid more toxic.
Technical Abstract: Resin acids constitute the most important group of acutely toxic chemicals to fish in waste waters of pulp mills; dehydroabietic acid (DHAA) is one of the most persistent and abundant. The acute toxicity of DHAA has been previously determined in rainbow trout Oncorhynchus mykiss however the effect of biotransformation enzyme manipulation on acute toxicity is not known. Piperonyl butoxide PBO and salicylamide SAL were utilized in the present study to determine their role in the acute toxicity of DHAA and their efforts on ethoxyresorufin O-deethylase EROD uridine diphspho-glucuronosyltransferase UDPGT Response substrate p nitrophenol despite residue analyses which indicated that SAL inhibited glucuronidation of DHAA. These results suggest that manipulation of glucuronidation detoxication by SAL has little or no effect on the acute toxicity of DHAA to rainbow trout. Piperonyl butoxide treatment induces EROD and increases toxicity suggesting that Phase I biotransformation has an important role in the acute toxicity of DHAA. In a separate experiment the effects of B-naphthoflavone BNF treatment on biomarker response was observed to