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IN VITRO EFFECTS OF BROMINATED FLAME RETARDANS ON CALCIUM BUFFERING MECHANISMS IN RAT BRAINS.
Citation:
COBURN, C. G., M. C. CURRAS-COLLAZO, AND PRASADA RAO S. KODAVANTI. IN VITRO EFFECTS OF BROMINATED FLAME RETARDANS ON CALCIUM BUFFERING MECHANISMS IN RAT BRAINS. Presented at International Society for Neurochemistry and American Society for Neurochemistry, Cancun, MEXICO, August 19 - 24, 2007.
Description:
Polybrominated diphenyl ethers (PBDEs) are widely used as additive flame-retardants and have been detected in human blood, adipose tissue, and breast milk. Developmental and long-term exposures to these chemicals may pose a human health risk, especially to children. It has been demonstrated that polychlorinated biphenyls (PCBs), which are structurally similar to PBDEs and cause neurotoxicity, perturb intracellular signaling events including calcium homeostasis and protein kinase C translocation, which are critical for the neuronal function and development of the nervous system. The objective of the present study was to test whether environmentally relevant PBDE congeners 47 and 99 are also capable of perturbing Ca2+ homeostasis. Calcium buffering was determined by measuring 45Ca2+-uptake by microsomes and mitochondria, isolated from adult male rat brain (frontal cortex, cerebellum, hippocampus and hypothalamus). Results
show that PBDEs 47 and 99 inhibit both microsomal and mitochondrial 45Ca2+ uptake in a concentration-dependent manner. The effect of these congeners on 45 Ca2+-uptake is similar in all four brain regions though the hypothalamus seems to be slightly more sensitive. Between the two organelles, the congeners inhibited mitochondrial 45Ca2+-uptake to a greater extent than microsomal 45Ca2+-uptake. These results indicate that PBDE 47 and PBDE 99 perturbed calcium signaling in rat brain in a similar manner as do PCBs suggesting a common mode of action of
these persistent organic pollutants. (This abstract does not necessarily reflect USEPA policy).