Oral supplementation of gossypin during lead exposure protects alteration in heme synthesis pathway and brain oxidative stress in rats.
OBJECTIVE
The objective was to study the efficacy of oral supplementation of gossypin, a flavonoid, during lead exposure in preventive alterations in the heme synthesis pathway, brain oxidation, and tissue lead uptake in rats.


METHODS
Male rats were used for the experiment and were exposed to lead (0.5% in drinking water) or lead plus oral supplementation of gossypin (25 or 100mg/kg) for 3 wk to determine the preventive effect of gossypin against lead toxicity. Animals were sacrificed after 3 wk for various biochemical variables suggestive of oxidative stress and heme synthesis pathway in addition to the concentration of lead in the blood and brain.


RESULTS
Exposure to lead produced significant inhibition in the activity of blood delta-aminolevulinic acid dehydratase accompanied by an increase in urinary delta-aminolevulinic acid and the levels of reactive oxygen species. There were significant alterations in the levels of glutathione, thiobarbituric acid-reactive substances, reactive oxygen species, and superoxide dismutase activity on lead exposure. Most of these alterations were significantly prevented by oral coadministration of gossypin, particularly at the dose of 100mg/kg.


CONCLUSIONS
The antioxidant and moderate chelating properties of oral gossypin suggest a promising role in use either as a nutritional supplement during lead exposure or as a complementary chelating agent during chelation therapy.
Gautam
Pratibha
P
Division of Pharmacology and Toxicology, Defence Research and Development Establishment, Gwalior, India.
Flora
S J S
SJ
D000622:Aminolevulinic Acid / Q000652:urine; D000818:Animals; D001921:Brain / Q000378:metabolism*; D001923:Brain Chemistry; D002374:Catalase / Q000032:analysis; D005419:Flavonoids / Q000008:administration & dosage*; D005978:Glutathione / Q000097:blood; D019803:Glutathione Disulfide / Q000032:analysis; D006418:Heme / Q000096:biosynthesis*; D007854:Lead / Q000032:analysis / Q000097:blood / Q000633:toxicity; D007855:Lead Poisoning / Q000378:metabolism / Q000517:prevention & control*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D000623:Porphobilinogen Synthase / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000032:analysis / Q000097:blood; D013482:Superoxide Dismutase / Q000032:analysis; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
D005419:Flavonoids; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D007854:Lead; D006418:Heme; D000622:Aminolevulinic Acid; C022944:gossypin; D002374:Catalase; D013482:Superoxide Dismutase; D000623:Porphobilinogen Synthase; D005978:Glutathione; D019803:Glutathione Disulfide