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Toxicological consequences of differential regulation of cytochrome p450 Isoforms in rat brain regions by phenobarbital

  1. Author:
    Upadhya, S. C.
    Chinta, S. J.
    Pai, H. V.
    Boyd, M. R.
    Ravindranath, V.

  2. Author Address

    Natl Brain Res Ctr, ICGEB Campus, New Delhi 110067, India. Natl Brain Res Ctr, New Delhi 110067, India. Natl Inst Mental Hlth & Neurosci, Dept Neurochem, Bangalore 560029, Karnataka, India. Natl Canc Inst, Ctr Canc Res, Mol Targets Drug Discovery Program, NIH, Ft Detrick, MD 21702 USA. Ravindranath V Natl Brain Res Ctr, ICGEB Campus, New Delhi 110067, India.
    1. Year: 2002
  2. Journal: Archives of Biochemistry and Biophysics
    1. 399
    2. 1
    3. Pages: 56-65
  4. Type of Article: Article
  1. Abstract:

    Cytochrome P4502B is an isoform of cytochrome P450 (P450) that is induced by the anticonvulsant drug phenobarbital. Here, we demonstrate the constitutive expression and predominant localization of CYP2B in neurons of rat brain. Administration of phenobarbital to rats resulted in selective induction of P450 levels in cortex and midbrain, while other regions were unaffected. Immunohistochemical localization of P4502B in brains of phenobarbital treated rats revealed localization of P4502B in neuronal cells, most predominantly the reticular neurons in midbrain. The anticancer agent 9-methoxy-N- methylellipticinium acetate (MMEA) has been shown to exhibit preferential neuronal toxicity in vitro. Pretreatment of rats with phenobarbital potentiated the toxicity of intrathecally administered MMEA in vivo, as seen by the degeneration of reticular neurons. Thus, induction of P450 in selective regions of brain by phenobarbital would profoundly influence xenobiotic metabolism in these regions, especially in clinical situations where phenobarbital is coadministered with other psychoactive drugs/xenobiotics. (C) 2002 Elsevier Science (USA).

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