Plant polyphenols inhibit benzoyl peroxide-induced superoxide anion radical production and diacylglyceride formation in murine peritoneal macrophages

Citation
A. Kaul et Kl. Khanduja, Plant polyphenols inhibit benzoyl peroxide-induced superoxide anion radical production and diacylglyceride formation in murine peritoneal macrophages, NUTR CANCER, 35(2), 1999, pp. 207-211
Citations number
22
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
ISSN journal
01635581 → ACNP
Volume
35
Issue
2
Year of publication
1999
Pages
207 - 211
Database
ISI
SICI code
0163-5581(1999)35:2<207:PPIBPS>2.0.ZU;2-N
Abstract
Naturally occurring plant polyphenols, which include ellagic acid (EA), tan nic acid (TA), caffeic acid (CA), and ferulic acid (FA), were tested for th eir superoxide anion radical (SOR)-scavenging activities. SOR were produced by interaction of the tumor promoter benzoyl peroxide ((BPO) with murine p eritoneal macrophages in vitro. The levels of SOR were assessed microscopic ally by counting the number of formazan-positive cells per 250 cells produc ed by the reduction of nitro blue tetrazolium. BPO at a concentration of 15 mu g/1.85 x 10(6) cells/0.5 ml induced maximum formation of SOR in residen t and thioglycollate-elicited cells. All the tested polyphenols were able t o inhibit the formation of SOR induced by the tumor promoter to a variable degree. Inhibition of BPO-induced SOR formation by polyphenols was in the f ollowing order: FA > TA > CA > EA. BPO stimulated the accumulation of diacy lglycerol (DAG) in resident and elicited macrophages with concurrent releas e of choline equivalents from macrophages. Polyphenols inhibited DAG accumu lation, which paralleled the inhibition of choline equivalent release. FA w as observed to be the most effective and EA the least effective inhibitor o f SOR formation, DAG accumulation, and release of choline equivalents. It i s likely that inhibition of SOR formation might be due to some interference in the cellular lipid metabolism and phospholipid equivalent deacylation a nd choline release.