Physiological response to lipid peroxidation in ischemia and reperfusion during carotid endarterectomy.
BACKGROUND
In this study we aimed to assess lipid peroxidation during carotid endarterectomy by the formation of PUFA hydroperoxides (PUFAHP) and isoprostanes (IP) and concomitant peroxisomal beta-oxidation as a physiological mechanism to limit their concentration. Two markers of peroxisomal beta oxidation have been evaluated, formation of 2,3 dinor from IP and conjugated esadecadienoic acid (CD 16:2) from peroxisomal beta-oxidation of conjugated linoleic acid (CLA), an unusual fatty acid present in small concentration in our diet and preferentially beta-oxidised in peroxisomes.The study was conducted on 30 patients undergoing carotid endarterectomy. Blood samplings were performed before, during endarterectomy in the "ischemic phase", and 30 seconds, 30 minutes and 2 hours after reperfusion.


RESULTS
The results showed that PUFAHP increased significantly after 30 min of reperfusion in patients with controlateral stenosis > 50%, and steeply decreased after 2 hour of reperfusion. Interestingly, IP increased in a similar fashion of PUFAHP but never significantly. Both ratios CD16:2/CLA and DIN/IP also increased significantly after 30 min of reperfusion to decrease thereafter.


CONCLUSIONS
Our data show that lipid peroxidation takes place only in patients with high controlateral stenosis and within 2 hours occurs a physiological response aimed to decrease IP and PUFAHP by increasing their catabolism in peroxisomes.
Banni
Sebastiano
S
Università degli Studi di Cagliari - Dipartimento di Biologia Sperimentale - Cittadella, Universitaria - 09042 Monserrato, Cagliari, Italy. banni@unica.it
Montisci
Roberto
R
Sanfilippo
Roberto
R
Finco
Gabriele
G
Sanna
Daniela
D
Giordano
Elena
E
Murru
Elisabetta
E
Cordeddu
Lina
L
Carta
Gianfranca
G
Banni
Donata
D
Marchi
Antonio
A
D000222:Adaptation, Physiological; D000368:Aged; D002374:Catalase / Q000378:metabolism; D003251:Constriction, Pathologic; D016894:Endarterectomy, Carotid / Q000009:adverse effects*; D005231:Fatty Acids, Unsaturated / Q000378:metabolism; D005260:Female; D006801:Humans; D028421:Isoprostanes / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D020675:Peroxisomes / Q000378:metabolism; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism*
D005231:Fatty Acids, Unsaturated; D028421:Isoprostanes; D002374:Catalase
Lipids. 2007 May;42(5):463-72
17476550
J Neurochem. 1992 Nov;59(5):1609-23
1402908
Prog Lipid Res. 1997 Mar;36(1):1-21
9373618
JAMA. 2005 Jul 6;294(1):56-65
15998891
Annu Rev Nutr. 2001;21:193-230
11375435
J Biol Chem. 1990 Mar 15;265(8):4369-73
2307669
J Pharmacol Exp Ther. 1997 Sep;282(3):1658-65
9316884
J Biol Chem. 1971 Sep 10;246(17):5254-63
5125749
Stroke. 2007 Jun;38(6):1946-8
17463314
Circulation. 1998 Feb 10;97(5):501-9
9490248
Biochim Biophys Acta. 2005 Sep 5;1736(1):61-6
16055372
J Biol Chem. 1999 Jan 15;274(3):1313-9
9880501
FEBS Lett. 1998 May 22;428(1-2):32-6
9645469
J Clin Invest. 1990 Apr;85(4):1173-81
2318972
J Appl Physiol (1985). 1991 Oct;71(4):1185-95
1757340
Biochim Biophys Acta. 2004 Jun 1;1682(1-3):120-7
15158763
JAMA. 2005 Mar 16;293(11):1338-47
15769967
Annu Rev Nutr. 2002;22:505-31
12055356
J Nutr. 2006 May;136(5):1222-8
16614408
Prostaglandins Leukot Essent Fatty Acids. 2009 May-Jun;80(5-6):279-87
19403295
Front Biosci. 2007 Jan 01;12:1318-28
17127384