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Sub‐vasoactive concentrations of extracts from Amazonian palm berry (Euterpe oleraceae Martius) protect coronary arteries from damage following external exposure to superoxide
Author(s) -
Bell David R,
Moon Haley J
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.718.2
Subject(s) - chemistry , coronary arteries , superoxide , botany , traditional medicine , biology , biochemistry , artery , medicine , enzyme
In chemical assays, extracts from the Amazonian palm berry ACAI ( Euterpe oleraceae Martius) exhibit the highest ORAC FL activity of any food yet reported with exceptional ability to scavenge O 2 − . However, it is not known whether these chemical properties translate into an ability of ACAI to protect living tissues from O 2 − mediated damage. Therefore we examined whether extracts from ACAI protected porcine coronary arteries from O 2 − mediated damage. Arterial rings from 6 pigs were incubated in sterile tissue culture media overnight for use in in vitro isometric vascular reactivity studies. Maximum relaxation and sensitivity to A23187 was impaired in rings exposed externally to O 2 − (400uM pyrogallol (Py) for 15 m) but markedly improved when rings were co‐exposed with 0.5mg/L of ACAI pulp extracted in either phosphate buffer (ACAI aq ) or DMSO (ACAI DMSO ). % Maximum relaxation and ‐logED 50, mean + sem, were C, 84±12%, 7.82±0.2; Py, 63±12%, 7.60±0.06; Py+ACAI aq , 88±6%, 7.88 + 0.13; Py+ACAI DMSO, 73± 13%, 7.75± 0.13, n=4). At 10x its oxidant protective concentration, ACAI extracted with either phosphate buffer, DMSO, DDH 2 O or EtOH caused <10% total relaxation of rings. Our results demonstrate that ACAI extracts at concentrations too low to directly alter vasoreactivity protect coronary arteries from damage following external exposure to oxygen radicals. Thus the oxygen radical neutralizing effect of ACAI rather than direct modulation of vascular relaxation is responsible for the protective effects of ACAI in arteries exposed to reactive oxygen species.