Extracellular calcium is required for the polychlorinated biphenyl-induced increase of intracellular free calcium levels in cerebellar granule cell culture

Toxicology. 1999 Aug 13;136(1):27-39. doi: 10.1016/s0300-483x(99)00052-9.

Abstract

Recent studies from the laboratory indicate that polychlorinated biphenyl (PCB) congeners can alter signal transduction and calcium homeostasis in neuronal preparations. These effects were more pronounced for the ortho-substituted, non-coplanar congeners, although the mechanisms underlying these effects are not clear. In the present study the time-course and concentration-dependent effects of coplanar and non-coplanar PCBs on intracellular free calcium concentration ([Ca2+]i) in cerebellar granule cell cultures were compared using the fluorescent probe fura-2. The ortho-substituted congeners 2,2'-dichlorobiphenyl (DCB) and 2,2',4,6,6'-pentachlorobiphenyl (PeCB) caused a gradual increase of [Ca2+]i while the non-ortho-substituted congeners 4,4'-DCB and 3,3',4,4',5-PeCB had no effect. The increase of [Ca2+]i produced by 2,2'-DCB was time- and concentration-dependent. Further studies examined possible mechanisms for this rise in [Ca2+]i. In contrast to the muscarinic agonist carbachol, the effects of 2,2'-DCB on [Ca2+]i were not blocked by thapsigargin and required the presence of extracellular calcium. The effects of ortho-substituted PCBs may depend on their ability to inhibit calcium sequestration as 2,2'-DCB significantly inhibited 45Ca2+-uptake by microsomes and mitochondria while 3,3',4,4',5-PeCB had no effect. In addition, 2,2'-DCB significantly increased the binding of [3H]inositol 1,4,5-trisphosphate to receptors on cerebellar microsomes, suggesting another possible mechanism by which ortho-substituted PCBs can mobilize [Ca2+]i. These results show that PCBs increase [Ca2+]i in vitro via a mechanism that requires extracelluar calcium, and support previous structure-activity studies indicating that ortho-substituted PCBs are more potent than non-ortho-substituted PCBs.

MeSH terms

  • Animals
  • Animals, Newborn
  • Calcium / metabolism*
  • Calcium Channels / metabolism
  • Carbachol / pharmacology
  • Cells, Cultured
  • Cerebellum / cytology
  • Cerebellum / drug effects*
  • Cerebellum / metabolism*
  • Dose-Response Relationship, Drug
  • Environmental Pollutants / toxicity*
  • Inositol 1,4,5-Trisphosphate Receptors
  • L-Lactate Dehydrogenase / metabolism
  • Microsomes, Liver / drug effects
  • Microsomes, Liver / metabolism
  • Mitochondria, Liver / drug effects
  • Mitochondria, Liver / metabolism
  • Muscarinic Agonists / pharmacology
  • Neurons / drug effects*
  • Neurons / metabolism*
  • Polychlorinated Biphenyls / toxicity*
  • Rats
  • Rats, Long-Evans
  • Receptors, Cytoplasmic and Nuclear / metabolism
  • Structure-Activity Relationship
  • Thapsigargin / pharmacology

Substances

  • Calcium Channels
  • Environmental Pollutants
  • Inositol 1,4,5-Trisphosphate Receptors
  • Muscarinic Agonists
  • Receptors, Cytoplasmic and Nuclear
  • Thapsigargin
  • Carbachol
  • Polychlorinated Biphenyls
  • L-Lactate Dehydrogenase
  • Calcium