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J.S. Russell

Publications and source records attributed to J.S. Russell.

2 recordsLinked to original sources

Blarina brevicauda as a biological monitor of polychlorinated biphenyls: Evaluation of hepatic cytochrome p450 induction

We assessed the value of short-tailed shrews ( Blarina brevicauda ) as a possible biomonitor for polychlorinated biphenyl pollution through measurement of the induction of hepatic cytochrome P450 and associated enzyme activities. First, we checked the inducibility of four monooxygenases (benzyloxyresorufin-O-dealkylase [BROD], ethoxyresorufin-O-dealkylase [EROD], methoxyresorufin-O-dealkylase [MROD], and pentoxyresorufin-O-dealkylase [PROD]) by measuring the activity of these enzymes in hepatic microsomes prepared from shrews injected with $-naphthoflavone ($NF) or phenobarbital (PB), typical inducers of cytochrome P4501A (CYP1A) and CYP2B enzyme families, respectively. Enzyme activity was induced in shrews that received $NF but not in shrews that received PB; PROD was not induced by either exposure. Later, shrews were exposed to a mixture of polychlorinated biphenyls (PCBs) (Aroclor 1242:1254, in 1:2 ratio) at 0.6, 9.6, and 150 ppm in food, for 31 d. Induction in these shrews was measured by specific enzyme activity (BROD, EROD, and MROD) in hepatic microsomes, by western blotting of solubilized microsomes against antibodies to CYP1A or CYP2B, and by duration of sodium pentobarbital-induced sleep. These three CYP enzymes were induced in shrews by PCBs at similar levels of exposure as in cotton rat ( Sigmodon hispidus ). Neither sleep time nor the amount of CYP2B family protein were affected by PCB exposure. Blarina brevicauda can be a useful biomonitor of PCBs that induce CYP1A, especially in habitats where they are the abundant small mammal.

Environmental Toxicology and Chemistry

Wildlife in a chemical world

Snapping turtles were collected by the Ohio State EPA from six locations in Ohio believed to have different contaminant concentrations. Previously we reported significant correlations among four hepatic microsomal dealkylases and CYP1A in these turtles. Herein we compare ethoxyresorufin-O-dealkylase (EROD) and methoxyROD (MROD) to tissue contaminant concentrations. For Fifty-four of these turtles, muscle, fat body and liver tissues were assessed for PCBs and 20 organochlorine analytes and hepatic microsomal dealkylases. Of the contaminants analyzed, only DDE, dieldrin, oxychlordane, trans-nonachlor and PCB 1260 were detected in >25% of each sample type. When EROD and MROD activities were compared to tissue values for these contaminants, they were found to correlate significantly only to DDE, dieldrin and trans-nonachlor. For an 18 female subset of these turtles, serum PCBs and organochlorine pesticides, egg, fat body and liver dioxins and furans, and hepatic microsomal dealkylases were assessed. EROD and MROD both correlated significantly to serum PCB 105, PCB 138 and DDE, and to egg total PCBs. EROD and MROD did not correlate significantly with liver dioxins and furans, but there were significant correlations between EROD and egg and fat body dioxins and furans, and MROD and fat body dioxins and furans. It is expected that CYP1A-type inducers such as certain PCBs, and halogenated dioxins and furans, but not organochlorine pesticides, would be inducers in turtles. Presumably the correlation of monooxygenase with organochlorine pesticides is fortuitous, and toxic equivalencies are being calculated using a number of systems.

Ohio