Lipid peroxidation and the use of emulsified propofol in laparoscopic surgery

Manataki, A.; Tselepis, Alexandros D.; Glantzounis, Georgios K.; Arnaoutoglou, Helen M.; Tsimoyiannis, Evangelos C.; Stavropoulos, Nikolaos A.

doi:10.1007/s004640090104

Cited by 21 publications

(14 citation statements)

References 23 publications

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“…Our results differ from the previous report that Vitamin E does not protect against changes caused by halothanehypoxia in guinea pigs (Durak et al, 1996). This could be attributed to the more effective chain breaking properties of propofol (Aarts et al, 1995), having been speculated that propofol may be a potentially useful chain-breaking antioxidant in clinical situations where it is coincidentally used as an anesthetic or sedative (Stratford and Murphy, 1998;Manataki et al, 2001).…”

Section: Discussioncontrasting

confidence: 86%

Halothane induces oxidative stress and NF-κB activation in rat liver: Protective effect of propofol

et al. 2006

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Section: Discussioncontrasting

confidence: 86%

Halothane induces oxidative stress and NF-κB activation in rat liver: Protective effect of propofol

et al. 2006

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“…1), and presents antioxidant properties that have been demonstrated in vitro and in vivo. Propofol has been reported to inhibit lipid peroxidation in various experimental models (Sayin, M. M., 2002;Manataki, A. D., 2001), to protect cells against oxidative stress, and to increase the antioxidant capacity of plasma in humans (Stratford, N., 1998;Hans, P., 1997). However, the precise propofol antioxidant mechanism at the cellular level has not been fully understood.…”

Section: Introductionmentioning

confidence: 98%

Propofol Inhibits Caspase-3 in Astroglial Cells: Role of Heme Oxygenase-1

Acquaviva¹,

Campisi²,

Raciti³

et al. 2005

CNR

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Several lines of evidence have extensively demonstrated that peroxynitrite plays a pivotal role in Central Nervous System (CNS) injuries. The present study was aimed at elucidating the molecular mechanism by which propofol attenuates peroxynitrite-mediated injury in the brain. Primary cultured astroglial cells were incubated for 18 h with a known peroxynitrite donor (SIN-1,3 mM) in the presence or absence of propofol (40 microM, 80 microM and 160 microM). The protective effects of propofol were evaluated by MTT cytotoxicity assay, LDH release, and caspase-3 activation by Western blot analysis. Appropriate propofol concentrations (ranging from 40 microM to 160 microM) significantly increased HO-1 expression and attenuated SIN-1-mediated cytotoxicity and caspase-3 activation. The protective effects of propofol were mitigated by the addition of tin-mesoporphirin (SnMP), a potent inhibitor of HO activity. The addition of a specific synthetic inhibitor of NF-kappaB abolished propofol-mediated HO-1 induction, suggesting a possible role for this nuclear transcriptional factor in our experimental conditions. These findings indicate that propofol attenuates peroxynitrite-mediated apoptosis in astroglial cells, a property that may be relevant in both physiological and pathological processes in the CNS.

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“…There have been numerous studies of the effects of anesthesia on cellular oxidative stress. Sevoflurane, 29 isoflurane, 30 and pentobarbital 31 are involved in triggering peroxynitrite formation, dysfunctioning polymorphonuclear neutrophils, and producing nitric oxide that results in compromised lipid peroxidation and free radical scavenging as reflected by elevated SOD activity and TBARS levels. Propofol alleviated compromised antioxidant capacity in humans anesthetized with isoflurane, suggesting that the choice of anesthetic agents may contribute to postoperative recovery and anesthesia efficacy may change depending on the surgical region or disease present 30 .…”

Section: Discussionmentioning

confidence: 99%

“…Sevoflurane, 29 isoflurane, 30 and pentobarbital 31 are involved in triggering peroxynitrite formation, dysfunctioning polymorphonuclear neutrophils, and producing nitric oxide that results in compromised lipid peroxidation and free radical scavenging as reflected by elevated SOD activity and TBARS levels. Propofol alleviated compromised antioxidant capacity in humans anesthetized with isoflurane, suggesting that the choice of anesthetic agents may contribute to postoperative recovery and anesthesia efficacy may change depending on the surgical region or disease present 30 . In the present experiment, the level of TBARS and SOD activity increased in response to xylazine and ketamine and data that support the oxidative stress effects of xylazine and ketamine anesthetics are available 32–34 …”

Section: Discussionmentioning

confidence: 99%

Evaluation of Free Radical Formation Associated With Diagnostic Ultrasound

Kartal

Kaya

Kavutçu

et al. 2008

Vet Radiology Ultrasound

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Our objective was to evaluate kidney antioxidant status in rats subjected to an ultrasound examination. Thirty rats were divided into five groups for injection of saline (S) or anesthetic (A), and application of ultrasound using different modes, B mode, pulsed wave Doppler, and continuous wave Doppler, under anesthesia. Ultrasound was performed on days 1, 3, and 5 relative to the initiation of the experiment. Rats were then scarified on day 6. The kidney tissue thiobarbituric acid reactive substance (TBARS) level and superoxide dismutase (SOD) activity were measured. Both TBARS level and SOD activity increased, 21% and 38%, respectively, due to anesthesia (P < 0.04 for both). SOD activity increased further by a factor of 1.2 in response to ultrasound examination (P < 0.05), whereas TBARS level was not affected by Doppler and continuous wave Doppler compared to anesthesia. Increases in the level of TBARS (P < 0.03) and SOD activity (P < 0.01) were greatest when B-mode ultrasound was employed. These substances did not increase further when continuous wave Doppler was employed. The peak-negative acoustic pressure (9.16 vs. 9.74 MPa) and frequency (3.57 vs. 6.95 MHz) for B mode and pulsed wave Doppler were greater than those for continuous wave Doppler (0.22 MPa and 1.96 MHz). The estimated mechanical indexes were 4.87, 3.70, and 0.15 for B mode, pulsed wave Doppler, and continuous wave Doppler, respectively. In conclusion, anesthesia may cause tissue damage as reflected by elevated lipid peroxidation and free radical formation and ultrasound examination may amplify tissue damage through mechanical effects caused by ultrasound absorption.

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Lipid peroxidation and the use of emulsified propofol in laparoscopic surgery

Abstract: Anesthesia with continuous propofol infusion in laparoscopic surgery has a significant scavenging action on the formation of free radicals and exerts its greatest antioxidant effect in patients >/=48 years of age.

Cited by 21 publications

References 23 publications

Halothane induces oxidative stress and NF-κB activation in rat liver: Protective effect of propofol

Halothane induces oxidative stress and NF-κB activation in rat liver: Protective effect of propofol

Propofol Inhibits Caspase-3 in Astroglial Cells: Role of Heme Oxygenase-1

Evaluation of Free Radical Formation Associated With Diagnostic Ultrasound

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