Chemiluminescence-HPLC assay of phosphatidylcholine hydroperoxide generated by ischemia-reperfusion in the liver of rats

Takayama, Fusako; Egashira, Toru; Kudo, Yoshikuni; Yamanaka, Yasumitsu

doi:10.1016/0006-2952(92)90688-f

Cited by 27 publications

(11 citation statements)

References 13 publications

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“…PCOOH has recently gained atten tion as a primary peroxidative product of phosphatidyl choline (PC), the most important functional lipid in the cell membrane (29). It has been reported that the PCOOH level in liver increases with an increase in the duration of ischemia and also increases in proportion to the duration of reperfusion (30). In the present study, we also observed an increase in the plasma PCOOH level upon administra tion of LPS.…”

Section: Discussionsupporting

confidence: 75%

Effect of Methylprednisolone on Plasma Lipid Peroxidation Induced by Lipopolysaccharide

Kouno

Egashira

Takayama

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-The effects of methylprednisolone succinate (MP) on plasma lipid peroxidation, plasma SOD activity and superoxide production in polymorphonuclear leukocytes (PMNs) induced by lipopolysac charide (LPS) were examined in rats in vivo and in vitro. In rats subjected to LPS treatment, plasma phosphatidylcholine hydroperoxide (PCOOH) levels significantly increased, and the plasma Cu,Zn-SOD activity decreased by about 75%. When rats were given 30 mg/kg of MP intravenously, MP suppressed the elevation of plasma PCOOH levels and partially inhibited the decrease in plasma Cu,Zn-SOD activity. MP also suppressed PMA-induced superoxide production in PMNs primed by LPS. In in vitro experiments, low concentrations of MP had no effect on NADPH-dependent lipid peroxidation, but 4 mM MP produced 50% inhibition. MP had little effect on PMA-induced superoxide production in PMNs primed by LPS. Moreover, MP had no radical-trapping effect on superoxide, hydroxyl radical and stable DPPH radical. These results suggest that the suppressive effect of plasma lipid peroxidation by MP is not due to radical trapping effects or preventive anti-oxidation, but may involve the suppression of the lipid chain reaction in liver membrane resulting from PMA-induced superoxide anions generated by PMNs.

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Section: Discussionsupporting

confidence: 75%

Effect of Methylprednisolone on Plasma Lipid Peroxidation Induced by Lipopolysaccharide

Kouno

Egashira

Takayama

et al. 1994

Japanese Journal of Pharmacology

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“…These results suggested that most important functional lipid in the cell membrane urinastatin has protective effect against free radical-in- [8]. By using chemiluminescent high performance duced lipid peroxidation probably by inhibiting proteliquid chromatography (CL-HPLC), PCOOH can be ases especially elastase, from polymorphonuclear leucomeasured with high sensitivity and specificity [9].…”

Section: Significant Decreased Concentrations Of Pcooh (P õmentioning

confidence: 98%

“…Urinastatin was injected twice intravenously These endotoxemia-induced free radicals probably through tail veins using 50,000 u/kg at 0 and 12 hr after damage the liver by lipid peroxidation reaction, thus CLP. SOD 90,000 u/kg and catalase 50,000 u/kg were producing high mortality [4,8,9,16]. Superoxide given subcutaneously just before CLP and every 3 hr (O r0 2 ), hydrogen peroxide (H 2 O 2 ), and hydroxyl radithereafter up to 24 hr.…”

Section: Toxemia the Pathogenesis Of This Clinical Manifesta-mentioning

confidence: 99%

Effects of Urinastatin and Free Radical Scavengers on Hepatic Lipid Peroxidation in Endotoxemia

Htwe

Suzuki

Ouchi

et al. 1996

Journal of Surgical Research

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“…Phosphatidylcholine hydroperoxide (PCOOH) has re cently gained attention as a primary peroxidative product of phosphatidylcholine (PC), the most important func tional lipid in the cellular membrane (9,11). We previous ly determined PCOOH levels in the liver and plasma of rats subjected to hepatic ischemia-reperfusion (12). Our results demonstrated that increased PCOOH concentra tions in the plasma and liver can reflect liver cell damage (12) and that plasma PCOOH levels can be used to assess tissue injury following oxidative stress and for the investi gation of drug efficacy (13).…”

mentioning

confidence: 99%

“…We previous ly determined PCOOH levels in the liver and plasma of rats subjected to hepatic ischemia-reperfusion (12). Our results demonstrated that increased PCOOH concentra tions in the plasma and liver can reflect liver cell damage (12) and that plasma PCOOH levels can be used to assess tissue injury following oxidative stress and for the investi gation of drug efficacy (13). We found that Dic Na sig nificantly suppressed the elevation of PCOOH levels in plasma due to hepatic ischemia-reperfusion injury, in vivo (13).…”

mentioning

confidence: 99%

Effect of Diclofenac, a Non-Steroidal Anti-Inflammatory Drug, on Lipid Peroxidation Caused by Ischemia-Reperfusion in Rat Liver

Takayama

Egashira

Yamanaka

1994

Japanese Journal of Pharmacology

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ABSTRACT-The present study investigated the effects of diclofenac sodium (Dic Na) on lipid peroxidation (LPO) and liver injury in ischemia-reperfused rats. LPO was estimated from the levels of phosphatidylcholine hydroperoxide (PCOOH), a primary peroxidative product of phosphatidylcholine. Hepatic ischemia-reperfusion induced significant elevation of plasma PCOOH and caused liver injury in rats. Rats were treated daily with Dic Na or a-tocopherol (a-toc.), p.o., for 5 days and once at 1 hr prior to induction of ischemia. Both substances prevented LPO from decreasing the plasma PCOOH level, and they significantly suppressed the elevation of serum GOT and LDH, in a dose-dependent manner. Dic Na was able to scavenge the stable free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH), but did not show radical-trapping ability for superoxide anion (02-) or hydroxyl radicals (• OH), nor a suppressive ability for the NADPH-dependent LPO of microsomes. In contrast, a-toc. trapped both DPPH and 02-, but not • OH , and it inhibited the NADPH dependent LPO in vitro. These results suggest that Dic Na may suppress liver injury caused by ischemia-reperfusion through stable radical scavenging and the inhibition of super oxide production in activated phagocytes, both of which may restrain the induction and progression of oxidative stress.

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Chemiluminescence-HPLC assay of phosphatidylcholine hydroperoxide generated by ischemia-reperfusion in the liver of rats

Cited by 27 publications

References 13 publications

Effect of Methylprednisolone on Plasma Lipid Peroxidation Induced by Lipopolysaccharide

Effect of Methylprednisolone on Plasma Lipid Peroxidation Induced by Lipopolysaccharide

Effects of Urinastatin and Free Radical Scavengers on Hepatic Lipid Peroxidation in Endotoxemia

Effect of Diclofenac, a Non-Steroidal Anti-Inflammatory Drug, on Lipid Peroxidation Caused by Ischemia-Reperfusion in Rat Liver

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