# VIT E, SELENIUM, AND FATTY ACID-DEPENDENT B(A)P OXIDATIO

> **NIH NIH R01** · PENNSYLVANIA STATE UNIVERSITY, THE · 1987 · $96,643

## Abstract

The primary objectives of the proposed research are to investigate the
effects of reduced antioxidant defense mechanism(s), in this case vitamin E
deficiency, selenium deficiency and a combination of each, on the
metabolism of benzy(a)Pyrene-7,8-dihydrodiol (BP-7,8-diol) via the
prostaglandin synthetase, and microsomal lipid peroxidation-mediated
cooxidation in the rat lung.  The hypothesis to be tested is that dietary
vitamin E and selenium can prevent the generation of extremely reactive
electrophilic intermediates, which may be mutagenic and/or carcinogenic,
from BP-7,8-diol during cyclooxygenase and microsomal lipid
peroxidation-dependent cooxidation.  The proposed experiments will be
conducted with mature male rats fed on chemically defined, purified diets
with documented deficiencies of vitamin E, selenium or both.  The specific
experimental tasks addressed in this proposal include 1) the determination
of in vitro lipid peroxidation potential of lung microsomes, 2) the
measurement of in vitro binding to protein and DNA of BP-7,8-diol
metabolites derived from cyclooxygenase and lipid peroxidation-dependent
cooxidation, 3) the analysis and quantitation of BP-7,8-diol metabolites
formed in the prostaglandin synthetase and lipid peroxidation-dependent
reactions and 4) an assessment of the effects of purified
selenium-dependent and selenium-independent-glutathione peroxidases on in
vitro binding of BP-7,8-diol metabolites to protein and DNA.  The research
methods to be employed include spectrophotometric and isotope assays for
measurment of enzyme activities, and liquid scintillation spectrometry,
thin-layer, and high pressure liquid-chromatographic techniques for the
analysis of BP-7,8-diol metabolites.  From the information obtained in
these studies insight will be gained to the understanding of the precise
mechanism(s) by which vitamin E and selenium might protect the lung against
tumors induced by the prostaglandin synthetase-mediated cooxidation of
chemical carcinogens.  Our long-term objectives are to investigate the
synergistic effects of oxidate stress such as ozone exposure on the
induction of lung cancer by environmental chemical carcinogens and the
protective mechanism(s) of dietary vitamin E and selenium supplementation.

## Key facts

- **NIH application ID:** 3175968
- **Project number:** 5R01CA037979-02
- **Recipient organization:** PENNSYLVANIA STATE UNIVERSITY, THE
- **SAM.gov UEI:** NPM2J7MSCF61
- **Principal Investigator:** C CHANNA REDDY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $96,643
- **Award type:** 5
- **Project period:** 1986-04-01 → 1989-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3175968

## Citation

> US National Institutes of Health, RePORTER application 3175968, VIT E, SELENIUM, AND FATTY ACID-DEPENDENT B(A)P OXIDATIO (5R01CA037979-02). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3175968. Licensed CC0.

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