Changes in the defense against free radicals in the liver and plasma of the dog during hypoxia and/or halothane anaesthesia

El-Bassiouni, E. A.; Abo-Ollo, Magda Mohamed; Helmy, Mai M.; S, Ismail; Ramadan, M.

doi:10.1016/s0300-483x(98)00045-6

Cited by 19 publications

(15 citation statements)

References 13 publications

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“…The fact that hepatic lipid peroxidation, measured by TBARS and chemiluminescence determination, was significantly increased in halothane-treated animals, confirms that in hypoxic conditions this volatile anesthetics can generate free radical intermediates which contribute to liver injury (El-Bassiouni et al, 1998;Dahan and Teppema, 2003). In addition to the presence of oxidative stress, we observed in animals receiving halothane an increased expression of iNOS.…”

Section: Discussionsupporting

confidence: 77%

“…In hypoxic conditions, volatile anesthetics, particularly halothane, cause formation of reactive oxygen species (ROS), leading to overwhelming of antioxidant defenses (El-Bassiouni et al, 1998), lipid peroxidation and mild liver damage (Dahan and Teppema, 2003). The mechanisms underlying halothane liver injury are not fully understood in spite of having been intensively studied, but it is generally admitted that a decrease in hepatic blood flow during halothane anesthesia may decrease the PO 2 available to hepatocytes and direct the metabolism of halothane along a reductive cytochrome P450-dependent pathway, with formation of free radical intermediates (Awad et al, 1996;Fujii et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2006

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Section: Discussionsupporting

confidence: 77%

Section: Introductionmentioning

confidence: 99%

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

et al. 2006

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“…On the effect of TZ anaesthesia the sheep became hypoxaemic at 30 and 60 min (P < 0.05) in our study (Table 1). Hypoventilation and hypoxia that usually accompany TZ anaesthesia could also be responsible for ROS generation (El-Bassiouni et al, 1998). For example, superoxide dismutase, another antioxidant enzyme is known to be inhibited by hypoxia (Liu et al, 1977); therefore, ROS production increases.…”

Section: Discussionmentioning

confidence: 99%

Effects of tiletamine-zolazepam anaesthesia on plasma antioxidative status and some haematological parameters in sheep

Ceylan

Aydılek

Ipek

2007

Acta Veterinaria Hungarica

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It is not clear whether the anaesthetic agents tiletamine and zolazepam have antioxidant or pro-oxidant effects. Therefore, this study was carried out to investigate the effects of tiletamine-zolazepam anaesthesia on oxidant/antioxidant status in blood plasma and on haematological parameters in 10 healthy Awassi ewes. The tiletamine-zolazepam combination was administrated in a dose of 7.5 mg/kg intramuscularly. The animals were spontaneously breathing air during the procedure. Blood samples were collected by jugular venipuncture before induction and at 30, 60, 120 min, 24 h and 3 days after anaesthesia. Malondialdehyde concentration, an index of lipid peroxidation, was higher at 30, 60, 120 min and 24 h (P < 0.05) than the baseline value in the plasma. The level of glutathione decreased (P < 0.05) at 30, 60 and 120 min, then returned to the baseline level. Beta-carotene concentration was lower (P < 0.05) than the baseline value during anaesthesia with the exception of its level at 120 min. Glutathione peroxidase and catalase activities decreased (P < 0.05) at the onset of anaesthesia, then returned to baseline values. There was no significant change in vitamin A level. Red blood cell count, haematocrit and haemoglobin concentration significantly decreased (P < 0.05) only at 30 min and thereafter they gradually returned to the baseline values. Based on the results tiletamine-zolazepam anaesthesia seems to accelerate lipid peroxidation and to impair the enzymatic antioxidant defence in the blood plasma.

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“…In vivo , hypoxia induces a time‐dependent decrease in reduced glutathione (GSH) and other cellular antioxidants, and an increase in lipid peroxidation end‐products in the liver (El‐Bassiouni et al ., 1998) as a result of the formation of reactive oxygen intermediates (ROI), such as superoxide anion (O 2 •− ) (Minor et al ., 1993; Caraceni et al ., 1995), hydrogen peroxide (H 2 O 2 ) (Matuschak et al ., 1996), and nitric oxide (NO • ) (Gess et al ., 1997). Theoretically, ROI could degrade P450 apoproteins directly as suggested by the fact that H 2 O 2 formed in the hemoprotein active centre may interact with the enzyme associated Fe 2+ leading to heme destruction and enzyme inactivation (Karuzina & Archakoz, 1994).…”

Section: Discussionmentioning

confidence: 99%

Effect of hypoxia alone or combined with inflammation and 3‐methylcholanthrene on hepatic cytochrome P450 in conscious rabbits

Kurdi¹,

Maurice²,

El‐Kadi³

et al. 1999

British J Pharmacology

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1 To investigate the e ect of moderate hypoxia alone or combined with an in¯ammatory reaction or after 3-methylcholanthrene (3MC) pre-treatment on cytochrome P450 (P450), conscious rabbits were exposed for 24 h to a fractional concentration of inspired O 2 of 10% (mean PaO 2 of 34 mmHg). Hypoxia decreased theophylline metabolic clearance (Cl M ) from 1.73+0.43 to 1.48+0.13 ml min 71 kg 71 (P50.05), and reduced (P50.05) the formation clearance of theophylline metabolites, 3-methylxanthine (3MX), 1-methyluric acid (1MU) and 1,3-dimethyluric acid (1,3DMU). Hypoxia reduced the amount of CYP1A1 and 1A2 but increased CYP3A6 proteins. 2 Turpentine-induced in¯ammatory reaction reduced (P50.05) the formation clearance of 3MX, 1MU, and 1,3DMU, and diminished the amount of CYP1A1, 1A2 and 3A6 proteins. However, when combined with hypoxia, in¯ammation partially prevented the decrease in Cl M , especially by impeding the reduction of 1,3DMU. The amount of CYP1A1 and 1A2 remained reduced but the amount of CYP3A6 protein returned to normal values. 3 Pre-treatment with 3MC augmented the Cl M by 114% (P50.05) due to the increase in the formation clearance of 3MX, 1MU and 1,3DMU. 3MC treatment increased the amount of CYP1A1 and 1A2 proteins. Pre-treatment with 3MC prevented the hypoxia-induced decrease in amount and activity of the P450. 4 It is concluded that acute moderate hypoxia and an in¯ammatory reaction individually reduce the amount and activity of selected apoproteins of the P450. However, the combination of hypoxia and the in¯ammatory reaction restores P450 activity to near normal values. On the other hand, pretreatment with 3MC prevents the hypoxia-induced depression of the P450.

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Changes in the defense against free radicals in the liver and plasma of the dog during hypoxia and/or halothane anaesthesia

Cited by 19 publications

References 13 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

Effects of tiletamine-zolazepam anaesthesia on plasma antioxidative status and some haematological parameters in sheep

Effect of hypoxia alone or combined with inflammation and 3‐methylcholanthrene on hepatic cytochrome P450 in conscious rabbits

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