Polybrominated diphenyl ethers and polybrominated biphenyls in sediment and floodplain soils of the Saginaw River watershed, Michigan, USA.

Despite known historical release of polybrominated biphenyls (PBBs; brominated flame retardants) into the Pine River (St. Louis, MI, USA), a tributary of the Tittabawassee River which subsequently forms the Saginaw River and flows into Saginaw Bay-Lake Huron, little is known about spatial patterns of sediment contamination by PBBs in this watershed. In this study, concentrations of two groups of brominated flame retardants, polybrominated diphenyl ethers (summation PBDE; BDE-28, -47, -66, -100, -99, -85, -154, -153, -138, and -209) and PBBs were measured in more than 120 floodplain soil samples, surface sediment samples, and sediment cores collected in 2004 from the Shiawassee River, the Saginaw River, and Saginaw Bay, Michigan.

Dioxin-like toxicity in the Saginaw River Watershed: polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in sediments and floodplain soils from the Saginaw and Shiawassee Rivers and Saginaw Bay, Michigan, USA.

Sediment and floodplain soils in the Saginaw River Watershed, Michigan, USA, have been demonstrated to be contaminated with a variety of organic compounds, including polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (PCDDs), and polychlorinated dibenzofurans (PCDFs). Existing data indicate that, at some locations, the contamination exceeds human health risk-based regulatory levels and ecological risk-based screening levels. In this study, concentrations of PCBs including non-ortho coplanar congeners, PCDDs, and PCDFs were measured in more than 120 sediment and floodplain soil samples collected from the Shiawassee River (a tributary of the Saginaw River), the Saginaw River, and Saginaw Bay, to determine the sources and magnitude of contamination, and to elucidate the contributions from individual contaminant groups to the overall 2,3,7,8-tetrachlorodibezo-p-dioxin equivalents (TEQs).

Cellular and learned tolerances to chlordiazepoxide hypothermia and ataxia.

Four groups of rats received chlordiazepoxide (CDP): a) intermittently, experiencing hypothermia and rotarod performance (RR) deficit after test doses (contingency); b) chronically, experiencing hypothermia and RR deficit after test doses; c) intermittently, RR preceding test doses and with protection against hypothermia afforded by exposure to heat lamps (nonexperienced, noncontingency); and d) chronically, RR preceding test doses and with protection against hypothermia. After 36 days of chronic CDP (groups 2 and 4) or vehicle (groups 1 and 3), all groups experienced RR and body temperature (BT) drug deficits after test doses of CDP at the postwithdrawal test. Group 1 but not group 3 was tolerant to peak hypothermia of the drug.

Cellular and learned tolerance to pentobarbital ataxia.

Pentobarbital was administered to 4 groups of rats: 1) intermittently before testing on the rotarod (RR) (experienced, EXP), 2) chronically (CHR) before testing on the RR (EXP), 3) intermittently (INT) after being tested on the RR (NONEXP), and 4) chronically (CHR) after being tested on the RR (NONEXP). On postchronic testing, Group 1 (INT/EXP) failed to show tolerance to the RR decrement, related to prechronic scores, while Group 3 (INT/NONEXP) actually showed an enhanced RR decrement. Group 2 (CHR/EXP) and Group 4 (CHR/NONEXP) both exhibited prominent tolerance to RR impairment at the postchronic test, with a nonsignificant trend for greater tolerance in Group 2.

Cellular and learned tolerances for pentobarbital hypothermia.

The development of behavioral tolerance to pentobarbital-induced hypothermia, as separable from cellular and metabolic tolerance, was established. Pentobarbital (PB) was administered to 4 groups of rats, 2 groups of which received intermittent (INT) IP PB treatment. One of these groups, INT/EXP, experienced the hypothermic (measured as rectal body temperature) drug effect after PB injection.