Effects of sphingosylphosphorylcholine against oxidative stress and acute lung injury induced by pulmonary contusion in rats.

BACKGROUND/PURPOSE: The goal of this study was to evaluate effects of exogenous sphingosylphosphorylcholine (SPC) administration on acute lung injury induced by pulmonary contusion in rats. METHODS: Eight animals were included in each of the following five groups: control, contusion, contusion phosphate-buffered solution (PBS), contusion SPC 2, contusion SPC 10. SPC was administered 3 days at a daily two different doses of 2 µm/ml and 10 µm/ml intraperitoneally. The severity of lung injury was determined by the neutrophil activation and histological and immunohistochemical changes in the lung. Malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione (GSH) were determined to evaluate the oxidative status in the lung tissue. RESULTS: Treatment with 2 µM SPC inhibited the increase in lung MDA and NO levels significantly and also attenuated the depletion of SOD, GPx, and GSH in the lung injury induced by pulmonary contusion. These data were supported by histopathological findings. The inducible nitric oxide synthase (iNOS) positive cells and apoptotic cells in the lung tissue were observed to be reduced with the 2 µM SPC treatment. But, the 10 µM SPC treatment did not provide similar effects. CONCLUSIONS: In conclusion, these findings suggested that 2 µM SPC can attenuate lung damage in pulmonary contusion by prevention of oxidative stress, inflammatory process and apoptosis. All these findings suggest that low dose SPC may be a promising new therapeutic agent for acute lung injury.

Prevention of cyclophosphamide-induced hemorrhagic cystitis by resveratrol: a comparative experimental study with mesna.

PURPOSE: Hemorrhagic cystitis (HC) is the most common urotoxic side effect of cyclophosphamide (CP). The aim of this study was to compare the classical efficacy of mesna (2-mercaptoethane sulfonate sodium) with three different doses of resveratrol (RES) on cyclophosphamide-induced HC in rats. METHODS: Forty-six male Sprague-Dawley rats were divided into six groups. Group 1 served as a negative control (sham). Five groups received a single dose of cyclophosphamide (150 mg/kg) intraperitoneally at the same time. Groups 2, 3, 4, 5, and 6 received only CP, CP + 20 mg/kg RES, CP + 40 mg/kg RES, CP + 80 mg/kg RES, and CP + classical protocol of three doses of mesna (30 mg/kg three times), respectively. Antioxidants, cytokines, and malondialdehyde levels were measured in all groups. In addition, histopathological alterations in tissues were examined. RESULTS: CP administration induced severe HC with marked edema, hemorrhage, and inflammation in group 2. RES 20 mg/kg showed meaningful protection against bladder damage compared to the control group. It was seen that RES 40 mg/kg gave weaker protection but RES 80 mg/kg was not found to be effective. CONCLUSION: In conclusion, marked bladder protection was found in 20 and 40 mg/kg RES applications compared to the control group, but this protection was weaker than with mesna.

Desferrioxamine effectively attenuates testicular tissue at the end of 3 h of ischemia but not in an equal period of reperfusion.

OBJECTIVE: To investigate the effect of desferrioxamine (DFX) on ipsilateral and contralateral testis damage caused by experimental testis torsion and detorsion. MATERIALS AND METHODS: Forty rats were divided into five groups (n = 8): control, torsion (T), torsion + desferrioxamine (T + DFX), torsion/detorsion (T/D), and torsion/detorsion + desferrioxamine (T/D + DFX). The right testes of the rats were subjected to torsion and detorsion for 3 h each. Thirty minutes before the application of torsion and detorsion, DFX (100 mg/kg) was administered intramuscularly. Blood samples and testicular tissues were examined using specific biochemical and histopathological methods. RESULTS: Ipsilateral and contralateral testis tissue glutathione levels in the T group decreased compared with the control and T + DFX groups. Plasma glutathione peroxidase activity in the T, T/D, and T/D + DFX groups was lower than in the control group. Plasma catalase activity in the T and T/D groups decreased compared with the control group. Ipsilateral mean seminiferous tubule diameter of the T group was lower than that of the T + DFX group. The ipsilateral mean testis biopsy scores in the T and T/D groups were lower than in the control group. CONCLUSION: The administration of DFX prior to torsion may be useful only for preventing ischemic damage in ipsilateral and contralateral testes.

Oxidant and antioxidant status in children with subacute sclerosing panencephalitis.

We analyzed serum alpha-tocopherol, beta-carotene, retinol, and ascorbic acid levels and malondialdehyde and reduced glutathione concentrations on erythrocyte and cerebrospinal fluid in 30 patients with subacute sclerosing panencephalitis to evaluate oxidant and antioxidant status. Serum alpha-tocopherol, beta-carotene, retinol, ascorbic acid levels, and erythrocyte and cerebrospinal fluid reduced glutathione concentrations were decreased; however, erythrocyte and cerebrospinal fluid malondialdehyde levels were increased in the patients. Cerebrospinal fluid malondialdehyde levels were different between clinical stages of the disease (P < .05). Higher cerebrospinal fluid malondialdehyde level was associated with the more severe clinical stage. A positive correlation was found between cerebrospinal fluid malondialdehyde level and clinical stages (r = 0.42; P < .05) and between erythrocyte malondialdehyde level and clinical stages (r = 0.40; P < .05). Our findings showed presence of oxidative damage in subacute sclerosing panencephalitis and that antioxidants were increased as defense mechanisms of the organism against oxidative damage.

Desferrioxamine reduces oxidative stress in the lung contusion.

Our hypothesis in this study is that desferrioxamine (DFX) has therapeutic effects on experimental lung contusions in rats. The rats were divided into four groups (n = 8): control, control+DFX, contusion, and contusion+DFX. In the control+DFX and contusion+DFX groups, 100 mg/kg DFX was given intraperitoneally once a day just after the contusion and the day after the contusion. Contusions led to a meaningful rise in the malondialdehyde (MDA) level in lung tissue. MDA levels in the contusion+DFX group experienced a significant decline. Glutathione levels were significantly lower in the contusion group than in the control group and significantly higher in the contusion+DFX group. Glutathione peroxidase (GPx) and superoxide dismutase (SOD) levels in the contusion group were significantly lower than those in the control group. In the contusion+DFX group, SOD and GPx levels were significantly higher than those in the contusion group. In light microscopic evaluation, the contusion and contusion+DFX groups showed edema, hemorrhage, alveolar destruction, and leukocyte infiltration. However, histological scoring of the contusion+DFX group was significantly more positive than that of the contusion group. The iNOS staining in the contusion group was significantly more intensive than that in all other groups. DFX reduced iNOS staining significantly in comparison to the contusion group. This study showed that DFX reduced oxidative stress in lung contusions in rats and histopathologically ensured the recovery of the lung tissue.

Royal jelly can diminish secondary neuronal damage after experimental spinal cord injury in rabbits.

The aim of this experimental study was to investigate the neuroprotective effect of Royal jelly (RJ) on traumatic spinal cord injury (SCI). Twenty-one New Zealand male rabbits, weighing between 2.5 and 3.0 kg were divided into three groups: Sham (no drug or operation, n = 7), Control (laminectomy+single dose of 1 ml/kg saline orally, after trauma; n = 7) and RJ (laminectomy+100mg/kg RJ, orally, after trauma, n = 7). Laminectomy was perfor med at T10 and balloon catheter was applied extradurally for traumatic SCI. Four and 24h after surgery, rabbits were evaluated according to the Tarlov scoring system. Blood, cerebrospinal fluid and tissue sample from spinal cord were taken for measurements of antioxidant status or detection of apoptosis. Four hours after SCI, all animals in control or RJ treated groups became paraparesic. Significant improvement was observed in RJ treated group, 24h after SCI, with respect to control. Traumatic SCI led to increase in the lipid peroxidation and decrease enzymic or non-enzymic endogenous antioxidative defense systems, and increase in apoptotic cell numbers. RJ treatment mostly prevented lipid peroxidation and also augmented endogenous enzymic or non-enzymic antioxidative defense systems. Again, RJ treatment significantly decreased the apoptotic cell number induced by SCI.

Serum and liver tissue bio-element levels, and antioxidant enzyme activities in carbon tetrachloride-induced hepatotoxicity: protective effects of royal jelly.

The liver is a vital organ, and its function is generally impaired by chemicals. Some natural compounds have a protective role against liver diseases such as royal jelly (RJ). To our knowledge, there are no data available on the effect of RJ therapy on the levels of bio-element metabolisms and antioxidant enzyme activities in the carbon tetrachloride (CCl(4))-induced liver damage. Therefore, in the present study, we have investigated the role of RJ therapy in the trace and major elements and antioxidant enzymes in CCl(4)-induced hepatotoxicity in rats. Antioxidant enzyme activities decreased in the CCl(4)-treated group more than they did in the sham and RJ-administered groups. Many bio-element levels were also reduced in only the CCl(4)-treated group. This showed that the depletion of trace elements was related to erythrocyte antioxidant enzyme activities. RJ administration clearly increased the trace and major element levels and antioxidant enzyme activities in RJ groups. RJ may be used as functional foods because of their naturally high antioxidant potential and rich element content.

Oxidant/antioxidant system markers and trace element levels in children with nutritional rickets.

OBJECTIVE: To determine the oxidative stress and trace element levels in vivo in patients with nutritional rachitism associated with vitamin D deficiency. MATERIALS AND METHOD: A total of 30 patients, 18 males and 12 females, were included in the study. Age, sex, medical history, vital, and physical examination findings of each patient documented at presentation were recorded. Serum calcium, phosphorus, alkaline phosphatase, parathormone, and 25-OH vitamin D levels, as well as oxidant and antioxidant system parameters and trace element levels were studied. After being diagnosed with rachitism, the patients were administered a single dose of 300,000 IU vitamin D by intramuscular injection. The same analyses were repeated post-treatment. Thirty children with normal anthropometric measurements were included as the control group. The analyses described above were performed only once for the control group. RESULTS: Serum calcium, phosphorus, alkaline phosphatase, parathormone, and 25-OH vitamin D levels were different between the controls and children in the patient group (p<0.001). Analysis of trace element levels demonstrated markedly lower pretreatment zinc levels for the patient group compared to the controls, with a statistically significant difference (p=0.001). Comparison of pretreatment oxidant and antioxidant system markers between the patient and control groups demonstrated higher values for vitamin C, ß-carotene, reduced glutathione, and superoxide dismutase in the control group, whereas MDA was higher in the patient group. CONCLUSION: The present study demonstrated increased oxidative stress, reduced antioxidant defence system in patients with nutritional rachitism, with reduced oxidative stress and a pronounced improvement in the antioxidant system with vitamin D treatment.

The roles of melatonin and vitamin E plus selenium in prevention of oxidative stress induced by naloxone-precipitated withdrawal in heroin-addicted rats.

The therapeutic effects of melatonin or vitamin E plus Se (vE + Se) on the restrain of the heroin withdrawal-induced oxidative stress were studied. For this, rats were divided into ten groups. The rats were injected by fixed or variable doses of heroin for 16 consecutive days, and naloxone was given 1 h after the last heroin injection. One hour after naloxone administration, some groups were treated with melatonin or vE + Se. After 1 h this, blood samples were taken, and the levels of malondialdehyde (MDA) and reduced glutathione (GSH) in whole blood, ascorbic acid, α-tocopherol, retinol, ß-carotene, nitrite, nitrate, and ceruloplasmin levels in the serum were measured. Our findings showed that, naloxone administration precipitated the heroin withdrawal. This also increased the level of MDA and decreased the levels of GSH in blood. Melatonin or vE + Se administration prevented the rise in MDA levels and increased the GSH levels. On the other hand, there were some significant differences between α-tocopherol, retinol, ß-carotene, nitrite, nitrate, and ceruloplasmin levels of experimental groups. Results of present study showed that heroin withdrawal increased the lipid peroxidation and depressed endogenous antioxidative systems. Additionally, melatonin or vE + Se administrations prevented lipid peroxidation and augmented endogenous antioxidant defense systems.

Antioxidant enzyme and element status in heroin addiction or heroin withdrawal in rats: effect of melatonin and vitamin E plus Se.

Heroin use, withdrawal syndrome, and heroin-related deaths are still the most serious public health problems. Antioxidants and bio-elements are essential for metabolism in living organisms. To our knowledge, there are no data about the effect of antioxidant therapy on the levels of bio-elements and antioxidant enzymes in the naloxone (NX)-induced heroin withdrawal syndrome. Therefore, in the present study for the first time, we have investigated the role of antioxidant therapy, melatonin, and vitamin E plus Se, on the trace and major elements and antioxidant enzymes in the heroin addiction or heroin withdrawal in rats. Glutathione peroxidase levels were increased and catalase levels were decreased in the all study groups when compared to the sham group. The level of superoxide dismutase (SOD) in the fixed dose of heroin (FDH) given group was lower; however, in the variable doses of heroin (VDH) given group SOD level was higher. Furthermore, in withdrawal syndrome, Fe, Mg, Mn, and Ti levels were diminished and Al, Ca, and Cu levels were increased in the FDH+NX group. Moreover, Mg, Mn, and Se levels were also diminished and Al level was increased in the VDH+NX group. In conclusion, our results obviously indicated that heroin effected both bio-element status and antioxidant enzyme activities and, exogenous melatonin or vE+Se therapy might relieve on the element and antioxidant enzyme the destructive activity caused by heroin.

Protective effect of Matricaria chamomilla on ethanol-induced acute gastric mucosal injury in rats.

The antiulcerogenic and antioxidant properties of Matricaria chamomilla L. (Compositae) hydroalcoholic extract (MCE) on ethanol-induced gastric mucosal injury were investigated in rats. After the induction of gastric mucosal injury, all groups were sacrificed; the gastric ulcer index was calculated, and malondialdehyde (MDA) and reduced glutathione (GSH) in whole blood and gastric tissue, and serum ascorbic acid, retinol, and beta-carotene levels were measured in all groups. Pretreatment with MCE at some doses significantly reduced gastric lesions. Again, some doses of MCE significantly reduced the MDA, and significantly increased GSH levels in gastric tissue or whole blood. Serum beta-carotene and retinol levels were significantly higher in the 200 mg/kg MCE-administered group with respect to control. As a result, MCE clearly has a protective effect against ethanol-induced gastric mucosal lesions, and this effect, at least in part, depends upon the reduction in lipid peroxidation and augmentation in antioxidant activity.

Protective potential of Royal Jelly against carbon tetrachloride induced-toxicity and changes in the serum sialic acid levels.

Royal Jelly (RJ) is used in the Turkish folk medicine for the treatment of number of disorders. The present study describes the hepatoprotective and antioxidant activities of the RJ against carbon tetrachloride (CCl(4))-induced acute liver damage. Sprague-Dawley rats were used for the experiment. CCl(4) (0.8 ml/kg; s.c.) and RJ (50, 100, 200mg/kg; orally) were given every other day, for 20 days. Malondialdehyde, reduced glutathione in whole blood and tissues; ceruloplasmin, sialic acid, ascorbic acid, retinol, ß-carotene and liver enzymes levels in serum were measured. Additionally, histopathological alterations in the liver were examined. RJ exerted the significant protective effect on liver damage as well as on oxidative stress induced by CCl(4), resulting in reduced lipid peroxidation and improved endogenous antioxidant defence systems. It also reduced the elevated levels of liver enzymes. Histopathological study further confirmed the hepatoprotective effect of RJ, when compared with the CCl(4) treated control groups. In conclusion, present study reveals biological evidence that supports the use of RJ in the treatment of chemical-induced hepatotoxicity.

Dantrolene can reduce secondary damage after spinal cord injury.

The aim of this experimental study was to investigate the possible protective effects of dantrolene on traumatic spinal cord injury (SCI). Twenty-four New Zealand rabbits were divided into three groups: Sham (no drug or operation, n = 8), Control (SCI + 1 mL saline intraperitoneally (i.p.), n = 8), and DNT (SCI + 10 mg/kg dantrolene in 1 mL, i.p., n = 8). Laminectomy was performed at T10 and balloon catheter was applied extradurally. Four and 24 h after surgery, rabbits were evaluated according to the Tarlov scoring system. Blood, cerebrospinal fluid and tissue sample from spinal cord were taken for measurements of antioxidant status or detection of apoptosis. After 4 h SCI, all animals in control or DNT-treated groups became paraparesic. Significant improvement was observed in DNT-treated group, 24 h after SCI, with respect to control. Traumatic SCI led to an increase in the lipid peroxidation and a decrease in enzymic or non-enzymic endogenous antioxidative defense systems, and increase in apoptotic cell numbers. DNT treatment prevented lipid peroxidation and augmented endogenous enzymic or non-enzymic antioxidative defense systems. Again, DNT treatment significantly decreased the apoptotic cell number induced by SCI. In conclusion, experimental results observed in this study suggest that treatment with dantrolene possess potential benefits for traumatic SCI.

Does dexmedetomidine reduce secondary damage after spinal cord injury? An experimental study.

The aim of this experimental study was to investigate the possible protective effect of dexmedetomidine (DEX) on traumatic spinal cord injury (SCI). Twenty-two New Zealand rabbits were divided into three groups: sham (no drug or operation, n = 6), Control [SCI + single dose of 1 mL saline intraperitoneally (i.p), after trauma; n = 8] and DEX (SCI + 1 microg/kg dexmedetomidine in 1 mL, i.p, after trauma, n = 8). Laminectomy was performed at T10 and balloon angioplasty catheter was applied extradurally. Four and 24 h after surgery, rabbits were evaluated by an independent observer according to the Tarlov scoring system. Blood, cerebrospinal fluid (CSF), tissue samples from spinal cord were taken for biochemical and histopathological evaluations. After 4 h of SCI, all animals in control or DEX treated groups became paraparesic. On the other hand, 24 h after SCI, partial improvements were observed in both control and DEX treated groups. Traumatic SCI leads to increase in the lipid peroxidation and decreases enzymatic or nonenzymatic endogenous antioxidative defense systems. Again, SCI leads to apoptosis in spinal cord. DEX treatment slightly prevented lipid peroxidation and augmented endogenous antioxidative defense systems in CSF or spinal cord tissue, but failed to prevent apoptosis or neurodeficit after traumatic SCI. Therefore, it could be suggested that treatment with dexmedetomidine does not produce beneficial results in SCI.

The effects of Panax ginseng and Spirulina platensis on hepatotoxicity induced by cadmium in rats.

Cadmium is an environmental and industrial cumulative pollutant that affects many organs, specially the liver. The protective effect of Spirulina platensis and Panax ginseng on cadmium-induced oxidative stress and hepatotoxicity was evaluated in adult female Wistar albino rats. At the end of the 1-month experimental period, all animals were fasted for 12h and liver samples were taken for the determination of malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and nitric oxide (NO) levels. S. platensis and P. ginseng treatments showed marked decrease lipid peroxidation and increase of the endogenous antioxidants levels. The cadmium-induced histopathological changes were also minimized with the tested extracts. These results suggest that S. platensis and P. ginseng might play a role in reducing the toxic effect of cadmium and its antioxidant properties seem to mediate such a protective effect.

High levels of oxidative stress in patients with advanced lung cancer.

BACKGROUND AND OBJECTIVE: The aim of this study was to investigate oxidative stress status in different stages and histological types of lung cancer. METHODS: Forty-nine lung cancer patients, who had not received any therapy, and 20 healthy subjects were chosen for the study. Lung cancer patients were divided into those with early stage or advanced stage disease. The tumour type was adenocarcinoma in 24 patients, squamous cell carcinoma in 21 and large cell carcinoma in four. We measured serum nitrite, nitrate, ascorbic acid, retinol, beta-carotene and ceruloplasmin levels, and whole-blood malondialdehyde, reduced glutathione levels and catalase activity in patients with non-small cell lung carcinoma and healthy subjects. RESULTS: Statistically significant differences between the patient group and the control group were detected for all biochemical parameters. Mean malondialdehyde, nitrite, nitrate and ceruloplasmin levels and catalase activity were significantly higher in the group with advanced stage disease than in the control group. Mean beta-carotene, ascorbic acid and reduced glutathione levels were significantly lower in the group with advanced stage disease than in the control group. Mean malondialdehyde and nitrite levels were significantly higher in the patients with squamous cell carcinoma than in those with adenocarcinoma, and mean malondialdehyde level was also significantly higher in patients with squamous cell carcinoma than in those with large cell carcinoma. CONCLUSIONS: These results suggest that with advancing stage of lung cancer, the levels of oxidative stress increase, while levels of antioxidant molecules decrease. Patients with squamous cell carcinoma have higher oxidative stress as reflected by higher levels of malondialdehyde and nitrite.

Antioxidative role of melatonin in organophosphate toxicity in rats.

Previous studies revealed that oxidative stress could be an important component of the mechanism of organophosphate (OP) compound toxicity. The aim of the present study was to investigate both prophylactic and therapeutic effects of melatonin against fenthion-induced oxidative stress in rats. Therefore, we determined the changes in the levels of reduced glutathione (GSH) and malondialdehyde (MDA) in the whole blood, brain, pectoral muscle, liver, lung, heart, kidney, pancreas, and jejunum. Also, the changes in the levels of serum nitrite and nitrate, ascorbic acid, retinal, b-carotene, and ceruloplasmin were measured. In addition, activities of enzymatic antioxidants superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) in erythrocyte of normal and experimental animals were measured. It was found that fenthion administration increased the levels of MDA in all tissues and decreased or increased the levels of GSH in some tissues. In comparison to nitrate, nitrite and ascorbic acid levels in the serum of experimental groups, there was no significant difference between groups. However, fenthion toxicity led to decrease in retinol and beta-carotene levels; melatonin administration significantly prevented this decrease. Serum ceruloplasmin level was increased due to fenthion administration, but prophylactic and therapeutic melatonin administration inhibited the increase in ceruloplasmin level of serum. There was no significant change in SOD levels in melatonin-administered groups. Melatonin modulates the fenthion-induced changes in the activities of GPx and CAT. In conclusion, the results of the current study revealed that OP toxicity, induced by fenthion, activated oxidant systems in all antioxidant systems in some tissues. Melatonin administration led to a marked increase in antioxidant activity and inhibited lipid peroxidation in most of tissues.

Effect of grape seed extract on lipid peroxidation, antioxidant activity and peripheral blood lymphocytes in rats exposed to x-radiation.

The present studies were designed to evaluate supplemental grape seed extract (GSE) and vitamin E supplements on lipid peroxidation, on antioxidant systems and peripheral blood lymphocytes in rats exposed to x-rays. Three groups of rats were investigated: a control group (CG) received intraperitoneal (i.p.) physiological serum 1 mL/day (n=10), i.p.; a vitamin E group (VG) received 50 mg/kg/day (n=10); an i.p. grape seed extract group received 50 mg/kg/day (n=10). Four weeks later, a 6 Gy radiation dose was given to the rats. Blood samples were taken 24 h later after irradiation and lymphocyte, malondialdehyde (MDA), reduced glutathione (GSH), nitrate, nitrite, reduced ascorbic acid, retinol, beta-carotene and ceruloplasmin concentrations were analysed. The levels of GSH (p<0.05), retinol (p<0.001), beta-carotene (p<0.05) and ceruloplasmin concentration (p<0.001) in the GSE group were found to be higher than in the control group but the level of MDA (p<0.001) and nitrite concentration (p<0.05) in rats supplemented with GSE were found to be lower than in the control group. The results indicate that GSE enhanced the antioxidant status and decreased the incidence of free radical-induced lipid peroxidation in blood samples of rats exposed to x-radiation. The antioxidant effect of GSE given to animals was more effective than vitamin E administered before whole-body irradiation in rats.

Beneficial effect of N-acetylcysteine against organophosphate toxicity in mice.

Recent studies showed that oxidative stress could be an important component of the mechanism of organophosphate (OP) compounds toxicity. The aim of present study was to investigate either prophylactic and therapeutic effects of N-acetylcysteine (NAC) against fenthion-induced oxidative stress in mice. Additionally, the effects on survival rates were investigated. Therefore, we determined the changes of the blood levels of glutathione (GSH), malondialdehyde (MDA), nitrite, and nitrate in blood or serum. Additionally, all animals were observed for 6 h and the survival rates were recorded. It was found that fenthion administration increased the levels of MDA, and decreased the levels of GSH, nitrite and nitrate. On the other hand, both prophylactic and therapeutic NAC treatment decreased the levels of MDA, and increased the levels of GSH, nitrite, and nitrate. The results showed that NAC is able to attenuate the fenthion-induced oxidative stress whereby NAC has not only prophylactic but also therapeutic activity in fenthion poisoning. On the other hand, we found that NAC can clearly improve survival rates in mice administered with an acute high dose of fenthion poisoning. In conclusion, NAC can decrease OP-induced oxidative stress and mortality rate, but the exact mechanism of its NAC protective effect needs to be explored further.

Beneficial effects of Foeniculum vulgare on ethanol-induced acute gastric mucosal injury in rats.

AIM: To examine the anti-ulcerogenic and antioxidant effects of aqueous extracts of Foeniculum vulgare (FVE) on ethanol-induced gastric lesions in rats. METHODS: FVE was administered by gavage at doses of 75, 150 and 300 mg/kg, and famotidine was used at the dose of 20 mg/kg. Following a 60 min period, all the rats were given 1 mL of ethanol (80%) by gavage. One hour after the administration of ethanol, all groups were sacrificed, and the gastric ulcer index was calculated; whole blood malondialdehyde (MDA) and reduced glutathione (GSH), serum nitrate, nitrite, ascorbic acid, retinol and beta-carotene levels were measured in all the groups. RESULTS: It was found that pretreatment with FVE significantly reduced ethanol-induced gastric damage. This effect of FVE was highest and statistically significant in 300 mg/kg group compared with the control (4.18 +/- 2.81 vs 13.15 +/- 4.08, P < 0.001). Also, pretreatment with FVE significantly reduced the MDA levels, while significantly increased GSH, nitrite, nitrate, ascorbic acid, retinol and beta-carotene levels. CONCLUSION: FVE has clearly a protective effect against ethanol-induced gastric mucosal lesion, and this effect, at least in part, depends upon the reduction in lipid peroxidation and augmentation in the antioxidant activity.