Medical ozone treatment on prevention of epidural fibrosis in the rat model.

Background/Aim: Epidural fibrosis is one of the problems that can be seen after spinal surgery. The aim of this study was to investigate the possible preventive role of medical ozone (O) treatment on epidural fibrosis. Materials and Methods: Twenty-four Sprague Dawley rats were randomly split into four groups: control (C), O, laminectomy (L), and L+O groups. Animals in the C group were sacrificed at the beginning of the experiment. The L and L+O groups had L procedure, while O treatment was supplied for the O and O+L groups. After 42 days of follow-up, for histological evaluation and biochemical measurements, the ratio of epidural fibrosis and catalase (CAT) with malondialdehyde (MDA) levels in serum, respectively, were analyzed in terms of statistical differences. Results: Histologically, a distinct difference was o bserved in the epidural space after O treatment. A significant difference in epidural fibrosis areas is found to be between the O, L, and O+L groups (P < 0,0001). There was no statistically significant difference between CAT and MDA levels that were obtained by spectrophotometric analysis. Conclusion: Histological results suggest that medical O treatment after L can be used as an alternative method to prevent epidural fibrosis. Further studies with wide cohorts and interval measures are required to detail the effects of doses.

Effect of different doses of pregabalin on skeletal muscle ischaemia-reperfusion injury in rats.

AIM/INTRODUCTION: Analgesic, anti-inflammatory and anti-apoptotic effects of pregabalin have been shown previously. In this study, we investigated the protective effect of different doses of pregabalin on skeletal muscle IR injury in rats. MATERIALS AND METHODS: 24 rats were randomly divided into 4 groups (Control, Ischaemia-Reperfusion (IR), IR-Pregabalin 50 mg, IR-Pregabalin 200 mg). Following IR, serum Ischemia Modified Albumin (IMA) and tissue Paraoxonase (PON) were studied and gastrocnemius muscle tissue was removed for histopathologic examination. RESULTS: Interstitial inflammation was higher in the IR group than in the control and Pregabalin 200 mg groups (p = 0.037, p = 0.037, respectively). Congestion was higher in the IR group than in the control, Pregabalin 50 and 200 mg groups (p = 0.001, p = 0.004, p = 0.004, respectively). PON was lower in the IR group than in the Control, Pregabalin 50 and 200 mg groups (p = 0.001, p = 0.007, p = 0.015, respectively). IMA was higher in the IR group than in the Control, Pregabalin 50 and 200 mg groups (p < 0.0001, all). CONCLUSION: We think that administration of pregabalin, more prominent at 200 mg, can reverse the injury that occurs in the skeletal muscle of IR-induced rats. Pregabalin can be safely used for analgesia in cases of IR (Tab. 2, Fig. 9, Ref. 41).

Investigation of argyrophilic nucleolar organizing region.

BACKGROUND: Ischemia/reperfusion (I/R) injury is a complex event frequently observed in vascular surgery and can cause functional and structural cell damage. Nucleolar-organizing regions (NORs) are sites of the ribosomal genes located on chromosomes and can be stained with silver when they are active. Thus these proteins are named as argyrophilic-NOR (AgNOR)-associated proteins. We aimed to investigate any possible effects of renal I/R injury on the NOR protein synthesis and association between the AgNOR proteins amount and histopathological injuring score. METHODS: Nine female wistar-albino rats with weight of 200-250g were included into the study. The animals were randomly divided in two groups, a Control Group and an I/R Group. In I/R group, rats were subjected to 45 minutes of renal pedicle occlusion followed by 24 hours of reperfusion. In the control group no drug injections or ischemia reperfusion were performed in animals. Then histopathological injury score, mean AgNOR number and total AgNOR area/nuclear area (TAA/NA) were detected for each rat. RESULTS: The differences between control and I/R groups were significant for histopathological injury scores (p = 0.016). Also the differences between control group and I/R group were significant for mean AgNOR number (p = 0.000) and TAA/NA ratio (p = 0.000). Additionally, there was a positive correlation between TAA/NA ratio and histopathological injury score (r = 0.728; p = 0.026) and between mean AgNOR number and histopathological injury score (r = 0.670; p = 0.048). CONCLUSION: The detection of AgNOR proteins amount may be used as an indicator to obtain information about the cellular behaviour (self-protective mechanism of tubular epithelial cells) against I/R injury and cellular damage levels (Tab. 2, Fig. 4, Ref. 24).

Vitamin C ameliorates high dose Dexmedetomidine induced liver injury.

BACKGROUND: We investigated whether vitamin C has protective effects on rat liver tissue treated with different dexmedetomidine doses. MATERIAL AND METHODS: Thirty five wistar albino rats were randomly divided into 5 groups (Control (0.9% NaCl intraperitoneally (i.p.), Dexmedetomidine 5 µg.kg(-1) (i.p.), Dexmedetomidine 5 µg.kg(-1) i.p. plus Vitamin C (100 mg.kg(-1)), Dexmedetomidine 10 µg.kg(-1) i.p. and Dexmedetomidine 10 µg.kg(-1) i.p. plus Vitamin C (100 mg.kg(-1)). Histopathological liver injury, superoxide dismutase (SOD) activity and tissue Malondialdehyde levels were investigated. RESULTS: Hepatocyte degeneration was significantly higher in D10 group than those in other study groups (p < 0.0001, p = 0.002, p < 0.0001, p = 0.005, respectively). Similarly, liver tissue sinusoidal dilatation and hepatocyte necrosis were significantly higher in D10 group than those in other groups (p < 0.0001, p < 0.0001, p = 0.002, p < 0.0001 and p < 0.0001, p = 0.046, p < 0.0001 and p = 0.002, respectively). Tissue MDA levels in D10 group were significantly higher than those in control, D5+Vit C and D10+Vit C groups (p = 0.028, p = 0.004, p = 0.031, respectively). SOD enzyme activity in D10 group was significantly lower than in control, D5+Vit C and D10+Vit C groups (p < 0.0001, p = 0.023 and p = 0.031, respectively). CONCLUSION: High dose dexmedetomidine can induce hepatic injury and oxidative stress in rats while pre-treatment with vitamin C may be effective in protecting liver tissue against this newly recognized undesirable dexmedetomidine effect (Tab. 2, Fig. 5, Ref. 30).

The protective effects of dexmedetomidine on hepatic ischemia reperfusion injury.

OBJECTIVE: The aim of this study was to evaluate the effect of dexmedetomidine (100 µg/kg-ip) on liver ischemia and reperfusion (I/R) in rats. METHODS: Twenty-four Wistar Albino rats were separated into three groups as control (C), ischemia-reperfusion injury (I/R) and dexmedetomidine group (I/R-D). Ischemia was induced with portal clampage for 45 minutes and reperfusion period was 45 minutes after declampage. Group I/R-D was received dexmedetomidine 100 µg/kg i.p. 30 min before portal clampage. Thiobarbutiric Acid-Reactive Substances (TBARS), glutathioneS-transferase (GST), superoxide dismutase (SOD), Catalase (CAT), and Paraoxonase 1 (PON-1) were investigated in blood samples. Also HSP60 and p53-positive hepatocytes were counted under ImageJ image analysis program. RESULTS: All parameters, except GST levels, were significant between the groups (p < 0.05). Although HSP60 expression was significantly increased between I/R, I/R-D and C groups there were no significant differences between I/R-D and C (p = 0.443). On the other hand, p53 expression was also significantly increased between I/R, I/R-D and C groups At the same time, there were no significant differences between I/R-D and C groups (p = 0.354). CONCLUSION: All the results suggest that dexmedetomidine has beneficial effects on liver ischemia/reperfusion stress (Tab. 1, Fig. 2, Ref. 49).

Oxidative stress and antioxidant activity of female rat liver tissue after sevoflurane anaesthesia: young versus old.

AIM: The aim of our study was to assess the evidence of oxidative stress in the rat liver tissue by studying enzymes, such as nitric oxide synthase (NOS), superoxide dismutase (SOD), glutathione-S transferase (GST) activity, and thiobarbutiric acid-reactive substances (TBARS) levels in young versus old female rats after sevoflurane anaesthesia. MATERIAL AND METHOD: The study involved 28 female Wistar Albino rats. The rats were divided into the two groups [(Group I, n=14): Young sevoflurane group (Group I-YS, n=7); Young control group (Group I-YC, n=7)], [(Group II, n=14): Old sevoflurane group (Group II-OS, n=7); Old control group (Group II-OC, n=7)]. Sevoflurane was administered at 2 % volume inspiratory concentration, 6 L.min-1 in 100 % O2 for 2 hours. The control groups were not subjected to any procedures. Accordingly, GST, SOD, and NOS enzyme activity and TBARS level, were studied in the liver tissue samples of the rats to determine the presence of oxidative stress (OS) and antioxidant activity. RESULTS: Following administration of sevoflurane anaesthesia; GST, SOD enzyme activity and TBARS level was significantly higher in the Group I-YS than in the Group I-YC and in the Group II-OS than in the Group II-OC. There was no difference between the groups when the mean NOS levels were compared. CONCLUSION: Although the results of our study are similar to the previous indicating that sevoflurane has the capacity to induce the oxidative stress; a new data has been recorded that sevoflurane has a similar effect on the OS level in aged and young female rat (Tab. 1, Fig. 4, Ref. 48).

Comparison of effects of anaesthesia with desflurane and enflurane on liver function.

INTRODUCTION: Although most general anaesthesia procedures are performed without any complications, volatile agents may have adverse effects on various living systems. This study aimed to compare the effects of desflurane and enflurane on liver function. METHODS: 40 patients, who were in the ASA I-III risk groups and were planned to undergo head and neck surgery of at least three hours' duration, were randomly divided into two groups: the desflurane (Group D) and enflurane groups (Group E). Venous blood samples (5 ml) of the patients were obtained before anaesthesia induction, in the postoperative first hour and on the first and seventh days. The samples were centrifuged and then stored at -80 degrees Celsius until the determination of glutathione S-transferase (GST) levels. For maintenance of anaesthesia in Group D, desflurane (6 percent) was used, while in Group E, enflurane (1.2 percent) was used. RESULTS: GST levels were significantly higher in Group E in the postoperative first hour (p-value is 0.002), and on the first day (p-value is 0.025) and seventh day (p-value is 0.035), although there were no differences preoperatively (p-value is more than 0.05). When postoperative levels were compared with preoperative levels, the postoperative GST levels of Group E were significantly higher (first hour [p-value is 0.008], first day [p-value is 0.010], seventh day [p-value is 0.038]). CONCLUSION: Subclinical hepatic injury after anaesthesia continues to be an issue of interest, particularly with the development of new, more sensitive methods of measuring GST levels. The increase in GST concentration after anaesthesia is thought to be a result of reduced hepatic blood flow. This study has shown that desflurane has fewer effects than enflurane on liver function tests in lengthy operations of up to 330 minutes.

Propofol and tourniquet induced ischaemia reperfusion injury in lower extremity operations.

BACKGROUND AND OBJECTIVE: Extremity surgery with tourniquet to provide a bloodless field may be a good human model for ischaemia reperfusion (IR) injury. The aim of this study was to investigate the effects of three different modes of propofol use on tourniquet induced IR injury in lower extremity operations. METHODS: Thirty-three consecutive ASA Grade I and II patients were randomized into three groups of 11 patients each. In the spinal group (Group S), after intrathecal anaesthesia, sedation was given with a propofol infusion at 2 mg kg-1 h-1 after a 0.2 mg kg-1 bolus dose and fentanyl 100 microg. In the general (Group G) and TIVA (Group T) groups, general anaesthesia was induced with propofol 2 mg kg-1 with fentanyl 100 microg and maintained with inhalation of halothane or infusion of propofol respectively. Venous blood samples were obtained at different time points for measurements of plasma malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels. RESULTS: Plasma MDA levels were increased significantly in the Group G at 1 min before tourniquet release and 5 and 20 min after tourniquet release compared with before induction of general anaesthesia (baseline). Before intrathecal anaesthesia and before induction of general anaesthesia significantly decreased levels of MDA were observed both before and after tourniquet release compared to baseline. Plasma SOD and CAT concentrations were decreased significantly only at tourniquet release in the Group G compared with baseline. In the Groups S and T these enzymes were not changed significantly. Plasma GPx levels were not altered in any groups. CONCLUSION: Propofol administration may inhibit lipid peroxidation and restore antioxidant enzyme levels in extremity surgery requiring tourniquet application.

Oxidant status in maternal and cord plasma and placental tissue in gestational diabetes.

The aim of this study was to measure oxidant/antioxidant status in maternal and cord plasma and in placental tissue in gestational diabetes and to correlate the results with the quality of glycemic control of the mother. To achieve this, blood and placental tissue samples have been obtained from pregnant women with gestational diabetes mellitus (GDM) and from the umbilical cord of their fetuses. The same samples have been collected from pregnant women without GDM. In all the samples, oxidant and antioxidant parameters have been studied. It has been observed that the antioxidant defense system was impaired; xanthine oxidase, which is the main free radical-producing enzyme (XO) in the living cells, was activated; and oxidation reactions were accelerated in the samples obtained from patients with GDM. Results suggest presence of oxidant stress in the gestational diabetes, the reason probably being impaired antioxidant defense mechanism and increased free radical production through XO activation.

Effects of garlic extract on oxidant/antioxidant status and atherosclerotic plaque formation in rabbit aorta.

BACKGROUND AND AIM: The results of a number of studies suggest that garlic (or garlic extracts) may have favourable effects against the development of atherosclerosis. The aim of this study was to investigate the effects of garlic extract supplementation on oxidant/antioxidant status and atherosclerotic plaque formation in rabbit aortic tissue. METHODS AND RESULTS: Twenty-two male New Zealand White rabbits were fed a cholesterol-supplemented diet (0.5 g/Kg/day) and nine control rabbits a regular diet for four months. At the end of this period, atherosclerotic plaque formation and antioxidant activity were measured in the aortic tissue of the controls and seven of the cholesterol-fed animals. Of the remaining 15 experimental animals, seven were fed normal laboratory diet and eight a normal diet plus garlic extract (1.5 ml/Kg/day) for a further three months before atherosclerotic plaque formation and antioxidant activity were measured in the aortic tissue of both groups. The cholesterol-fed animals showed a significantly impaired antioxidant system associated with increased plaque formation. However, garlic extract supplementation significantly improved antioxidant status and reduced the plaque surface area. CONCLUSIONS: In this experimental model, garlic extract dietary supplementation activated the antioxidant system and decreased peroxidation in aortic tissue. There was also a reduction in atherosclerotic plaque area. Although further studies are required to elucidate the mechanisms involved, the protective activity of garlic extract may be due to its antioxidant properties.

Effects of isoflurane on nitric oxide metabolism and oxidant status of guinea pig myocardium.

BACKGROUND: Volatile anesthetics (VAs) have been shown to enhance myocardial recovery during reperfusion, the mechanism of which has not been clarified yet. It has been supposed that this effect of VAs may appear through antioxidative mechanisms. METHODS: Thirty guinea pigs were used in the study. There were three groups with 10 animals in each: I - control, II - isoflurane+oxygen and III - oxygen. Isoflurane (2.0% v/v) and oxygen (100%) mixture was given to the animals via a face mask in the isoflurane+oxygen group at the rate of 21 per min for 30 min a day for three consecutive days. In the oxygen group, oxygen alone (100%) was given under the same conditions as in the isoflurane+oxygen group. At the end of the experiments, the animals were killed and their hearts were removed. In the heart tissues, nitric oxide synthase (NOS) activity, nitric oxide (NO) pool (NO*+NO2-) and malondialdehyde (MDA) levels were measured. RESULTS: NOS activity was found to be higher and the NO pool lower in the isoflurane+oxygen group compared with those of control and oxygen groups. In the oxygen group, MDA level was found to be higher compared to the other groups. There was, however, no significant difference between MDA levels of the control and isoflurane+oxygen groups. CONCLUSION: Our results suggest that isoflurane prevents peroxidation reactions in heart tissue, possibly by scavenging toxic oxygen radicals produced under hyperoxygenation conditions as occurs with general anesthesia.

Reduced antioxidant defense capacity in myocardial tissue from guinea pigs treated with 5-fluorouracil.

Antioxidant defense capacity was investigated in myocardial tissue from guinea pigs treated with 5-fluorouracil (5-FU) at a dose of 400 mg/kg/d daily for 5 d administered intraperitonally. Treatment with 5-FU lowered the activities of cardiac superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) accompanied by higher catalase (CAT) activity. Further, antioxidant potential (AOP) values were lower but oxidation resistance (OR) and malondialdehyde (MDA) levels were higher in the 5-FU-treated tissue. With regard to myocardial iron (Fe) and copper (Cu) levels, no significant differences were found between the groups. Results suggest that 5-FU treatment causes impairment in the myocardial antioxidant defense system and leads to cardiac peroxidation. It has been postulated that these changes might be responsible for the 5-FU cardiotoxicity seen in some patients, and antioxidant therapy might provide a therapeutic advantage.

In vitro effects of selected flavonoids on the 5'-nucleotidase activity.

A series of structurally related flavonoids and related compounds were evaluated whether they have inhibitory properties on the 5'-nucleotidase (5'-ribonucleotide phosphohydrolase; EC 3.1.3.5, 5'-NT) activity. Some of the flavonoids tested inhibit the enzyme such as quercetin, morin, apigenin, chrysin, myricetin, luteolin, diosmetin, (+/-)naringenin and diosmin. Rutin, naringin, hyperosid, (+/-)catechin, caffeic acid and rosmarinic acid had no inhibitory effect on the 5'-NT activity. Myricetin and quercetin were the most potent inhibitors for 5'-NT with IC50 values of 1.1 and 1.4 microM, respectively. Kinetic analysis showed a mixed type of inhibitor for both myricetin (Ki = 1.5 microM at pH 7.45), and quercetin (Ki = 0.6 microM at pH 7.45). The K(m) value for 5'-adenosine monophosphate (5-AMP) was determined with 77 microM at pH 7.45. The differential inhibitory potencies of flavonoids seem to be structurally related (hydroxylation pattern). The results demonstrate that some flavonoids are strong inhibitors of 5'-NT activity which can be correlated to their pharmacological effects.

Activities of the enzymes participating in purine and free-radical metabolism in cancerous human colorectal tissues.

Activities of adenosine deaminase, 5'-nucleotidase, xanthine oxidase, superoxide dismutase, glutathione peroxidase and catalase enzymes were measured in cancerous and non-cancerous adjacent colorectal tissues from 10 patients. Activities of DNA turn-over enzymes (ADA, 5'NT and XO) were found increased and those of free-radical metabolizing enzymes (SOD, GSH-Px and CAT) decreased in cancerous tissues compared with those of non-cancerous adjacent ones. Malondialdehyde (MDA) concentrations in cancerous tissues were also found higher than those of non-cancerous tissues, which indicated accelerated lipid peroxidation in the cancerous tissues. In the correlation analysis, disordered enzymatical relations were observed between the enzymes of both metabolic pathways. Results suggest that activities of purine metabolizing enzymes increase to cope with accelerated purine metabolism in cancerous tissues and, enzymatic antioxidant defense potential of cancerous tissues decreases due to carcinogenic processes in the tissues. Reduced antioxidant defense system makes the cancerous tissue more vulnerable to toxic effects of some free-radical species.

Impaired antioxidant defence in guinea pig heart tissues treated with halothane.

PURPOSE: To investigate the effects of halothane and halothane plus vitamin E treatment on myocardial free radical metabolism in guinea pigs. METHODS: Four groups of seven animals were studied: control, halothane, halothane plus vitamin E and vitamin E groups. In the halothane group, halothane 1.5% in oxygen was given for 90 min over three days. In the halothane plus vitamin E group, 300 mg.kg-1.day-1 vitamin E im was started three days before the first halothane treatment and continued for three days. Following sacrifice, the hearts were assayed for superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) and malondialdehyde (MDA) level was determined. Electron spin resonance (ESR) analysis and electron microscopy (EM) were also performed. RESULTS: In the halothane group, SOD activities and MDA concentrations were increased compared with control and GSH-Px and CAT activities were decreased. In the halothane plus vitamin E group, there were no differences in enzyme activity compared with halothane alone but the MDA level was decreased. In the vitamin E group, enzyme activities were increased compared with control. Mainly the CF3CHCl radical was identified by ESR analysis in heart tissues exposed to halothane and the concentration of this radical was reduced by vitamin E. Electron microscopy showed cytoplasmic vacuolisation and dilation in sarcoplasmic reticulum in the heart tissues exposed to halothane: both were prevented by vitamin E. CONCLUSION: Although halothane causes impairment in enzymatic antioxidant defence potential, due to lowered GSH-Px and CAT activity, and accelerates peroxidative reactions in the tissues affected, no subcellular damage occurred. Vitamin E may protect tissues against free radical attack by scavenging toxic free radicals formed in heart tissue during halothane anaesthesia.

Activity of the enzymes participating in purine metabolism of cancerous and noncancerous human kidney tissues.

In this study, activity of some of the key enzymes participating in purine metabolism was measured in cancerous and noncancerous human kidney tissues from 18 patients with renal cell carcinoma. Twelve cancerous tissues were at stage T1-T2 and 6 tissues were at stage T3-T4. Adenosine deaminase (ADA) and guanase (GUA) activity was increased and xanthine oxidase (XO) activity decreased in cancerous tissues compared to noncancerous ones. No difference was, however, found between 5'-Nucleotidase (5'-NT) activity of the tissues. There were also no statistically meaningful differences between the enzyme activities of the cancerous tissues at stage T1-2 and T3-4. Results suggest that the changes observed in the activity of the enzymes participating in purine metabolism result from accelerated DNA turnover in the cancerous tissues and cells, and these changes might provide selective advantage, possibly by causing acceleration of salvage pathway activity, to the cancer cells to grow and develop more rapidly.

Activities of superoxide dismutase and glutathione peroxidase enzymes in cancerous and non-cancerous human kidney tissues.

The activities of superoxide dismutases (total, cytoplasmic and mitochondrial) and glutathione peroxidase were measured in 10 cancerous and 10 non-cancerous adjacent human kidney tissues. Total (T-SOD) and cytoplasmic (Cu, Zn-SOD) superoxide dismutase and glutathione peroxidase (GSH-Px) activities were found lower in cancerous tissues compared with those of non-cancerous ones. However, no difference was found between the mitochondrial (Mn-SOD) superoxide dismutase activities of the tissues. Similarly, no differences were observed between the enzyme activity values of the tissues at stage I-II and III-IV renal cancer. In correlation analysis the positive relation found between Cu, Zn-SOD and GSH-Px enzymes in the non-cancerous tissues was found to be absent in the cancerous ones. The results suggest that enzymatic free radical defense mechanism is significantly reduced in the cancerous human kidney tissues due to depressed Cu, Zn-SOD and GSH-Px activities.

The effects of gentamicin on the activities of glutathione peroxidase and superoxide dismutase enzymes and malondialdehyde levels in heart tissues of guinea pigs.

In this study, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and malondialdehyde (MDA) levels were measured in heart tissues from guinea pigs treated with gentamicin and gentamicin plus vitamin E combination. Mean values were compared with those of the controls treated with only physiological saline solution. The activities of SOD and GSH-Px were found to be lower and the MDA level higher in the hearts from gentamicin-treated animals compared with those of the controls. In the gentamicin plus vitamin E group, however, tissue SOD activity was found to be increased and MDA level decreased significantly relative to the gentamicin group. GSH-Px activity was lowest in this group. Results suggest that gentamicin suppresses SOD and GSH-Px activities in heart tissue, thereby making the tissue more vulnerable to oxidative stress and peroxidative attacks, an important indicator of which is increased MDA level in the heart tissues from gentamicin-treated guinea pigs. This effect might be deleterious when gentamicin is used after cardiac surgery since a potential risk of free radical injury exists in the heart tissue during and/or after cardiac surgery owing to ischaemia and reperfusion processes, and, possibly, in the management of the patients with certain types of heart disease. Our results showed that vitamin E given concomitantly with gentamicin could protect the heart tissue against free radical injury.

The effects of gentamicin and vitamin E on enzymatic antioxidant defence in guinea-pig lung.

OBJECTIVE: To study the possible effects of gentamicin on the enzymic free-radical defence system in the lung. METHOD: Activities of cytoplasmic superoxide dismutase (CuZn-SOD), mitochondrial superoxide dismutase (Mn-SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) enzymes were studied in lung tissues from gentamicin-treated guinea-pigs compared to controls. RESULTS: Levels of those enzymes were higher in the gentamicin group except for xanthine oxidase (XO) activity. Vitamin E given concomitantly with gentamicin caused significant decreases in CuZn-SOD, Mn-SOD and GSH-Px activities but an increase in CAT activity in the lung tissue. Only vitamin treatment caused significant decreases in the activities of CuZn-SOD, Mn-SOD and GSH-Px enzymes and an increase in CAT activity. CONCLUSION: The results suggest that lung tissue is able to respond quickly and effectively against the adverse effects of some oxidant substances by inducing and/or activating the enzymatic free-radical defence system.