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DECREASED HEART RATE IS ASSOCIATED WITH CARBAMATE-INDUCED ACTIVATION OF PRO-INFLAMMATORY SERUM PROTEINS.
Citation:
MACK, C. M., P. BECKER, AND C. J. GORDON. DECREASED HEART RATE IS ASSOCIATED WITH CARBAMATE-INDUCED ACTIVATION OF PRO-INFLAMMATORY SERUM PROTEINS. Presented at Experimental Biology, San Francisco, CA, April 01 - 04, 2006.
Description:
Previously we reported that chlorpyrifos (CHP), an irreversible cholinesterase (ChE) inhibitor, induces hypertension in rats. Concomitant with hypertension, we found an increase in C-reactive protein, macrophage inflammatory protein-2 , monocyte chemotactic protein-5 and interferon-?. This study investigated the effects of carbaryl (CAR), a reversible ChE inhibitor on heart rate (HR), core body temperature (Tc) and pro-inflammatory protein expression. Adult, male LE rats (n=20) were implanted with telemetry units for ECG and Tc recording. Rats were dosed with CAR (75 mg/kg) or corn oil, (po). CAR induced an initial, transient increase in HR that was followed by a significant reduction that persisted for 8 hrs. CAR initially decreased Tc by 2.0 0 C which recovered within 11 hrs. Rats were euthanized 24 hrs after CAR or corn oil, and a multiplexed multi-analyte profile (MAP) of serum was performed. CAR exposure activated fibrinogen, apo-A1, endothelin, and Il-1?. Overall, both CHP and CAR alter hematologic biomarkers, however their expression profiles indicate potential mechanistic differences. These results offer further evidence that anti-ChE environmental neurotoxicants activate pro-inflammatory pathways associated with cardiovascular dysfunction. This abstract does not necessarily reflect US EPA policy.
Previously we reported that chlorpyrifos (CHP), an irreversible cholinesterase (ChE) inhibitor, induces hypertension in rats. Concomitant with hypertension, we found an increase in C-reactive protein, macrophage inflammatory protein-2 , monocyte chemotactic protein-5 and interferon-?. This study investigated the effects of carbaryl (CAR), a reversible ChE inhibitor on heart rate (HR), core body temperature (Tc) and pro-inflammatory protein expression. Adult, male LE rats (n=20) were implanted with telemetry units for ECG and Tc recording. Rats were dosed with CAR (75 mg/kg) or corn oil, (po). CAR induced an initial, transient increase in HR that was followed by a significant reduction that persisted for 8 hrs. CAR initially decreased Tc by 2.0 0 C which recovered within 11 hrs. Rats were euthanized 24 hrs after CAR or corn oil, and a multiplexed multi-analyte profile (MAP) of serum was performed. CAR exposure activated fibrinogen, apo-A1, endothelin, and Il-1?. Overall, both CHP and CAR alter hematologic biomarkers, however their expression profiles indicate potential mechanistic differences. These results offer further evidence that anti-ChE environmental neurotoxicants activate pro-inflammatory pathways associated with cardiovascular dysfunction. This abstract does not necessarily reflect US EPA policy.