Increased Levels Of Lipid Peroxidation Research Articles

Manganese pre-treatment attenuates cadmium induced hepatotoxicity in Swiss albino mice

Cadmium (Cd) is a soft, malleable bluish-white metal with low melting point, a ubiquitous heavy metal and an environmental pollutant, found in soil, water and air. The presence of Cd in the components of the environment such as air, soil and groundwater is to a large part due to human activity, and the general population is exposed mainly by contaminated drinking water or food. Manganese (Mn) is a component in many enzymes, which play an important role in counteracting oxidative stress. In vitro experiments have revealed the ability of Mn to scavenge oxygen free radicals generated in differently mediated lipid peroxidation (LPO) conditions. The aim of the present study was to investigate the in vivo preventive effect of Mn2+ pre-treatment on acute Cd-intoxication with regard to oxidative stress biomarker and antioxidant defense system in liver of Swiss albino mice. On exposure to Cd a significant increase in LPO levels, decrease in thiol content and induction in glutathione metabolizing enzyme were observed. Mn pre-treatment attenuated the modulation caused in the above-mentioned parameters due to acute Cd exposure in mice. In conclusion, the results from this study demonstrate that the protective effect of Mn in Cd-induced systemic toxicity in mice. Further investigations are required on the relation between Mn accumulation and resistance to oxidative stress and on the factors influencing Mn/Cd transport in rodents are needed to elucidate the molecular basis of this protective effect.

Biochemical effects of glyphosate based herbicide, Excel Mera 71 on enzyme activities of acetylcholinesterase (AChE), lipid peroxidation (LPO), catalase (CAT), glutathione-S-transferase (GST) and protein content on teleostean fishes

Effects of glyphosate based herbicide, Excel Mera 71 at a dose of 17.20mg/l on enzyme activities of acetylcholinesterase (AChE), lipid peroxidation (LPO), catalase (CAT), glutathione-S-transferase (GST) and protein content were measured in different tissues of two Indian air-breathing teleosts, Anabas testudineus (Bloch) and Heteropneustes fossilis (Bloch) during an exposure period of 30 days under laboratory condition. AChE activity was significantly increased in all the investigated tissues of both fish species and maximum elevation was observed in brain of H. fossilis, while spinal cord of A. testudineus showed minimum increment. Fishes showed significant increase LPO levels in all the tissues; highest was observed in gill of A. testudineus but lowest LPO level was observed in muscle of H. fossilis. CAT was also enhanced in both the fishes, while GST activity in liver diminished substantially and minimum was observed in liver of A. testudineus. Total protein content showed decreased value in all the tissues, maximum reduction was observed in liver and minimum in brain of A. testudineus and H. fossilis respectively. The results indicated that Excel Mera 71 caused serious alterations in the enzyme activities resulting into severe deterioration of fish health; so, AChE, LPO, CAT and GST can be used as suitable indicators of herbicidal toxicity.

Ursolic acid ameliorates carbon tetrachloride-induced oxidative DNA damage and inflammation in mouse kidney by inhibiting the STAT3 and NF-κB activities.

Ursolic acid (UA), a common pentacyclic triterpenoid compound, has been reported to have many benefits and medicinal properties. However, its protective effects against carbon tetrachloride (CCl4) induced injury in kidneys are not yet clear. In the current report, we investigated whether UA inhibited the oxidative stress and inflammation in the kidneys of CCl4 treated mice. Male ICR mice were injected with CCl4 with or without UA co-administration (25 and 50mg/kg intragastrically once daily) for six weeks. Our data showed that UA significantly prevented CCl4-induced nephrotoxicity in a dose-dependent manner, indicated by both diagnostic indicators of kidney damage and histopathological analysis. Moreover, CCl4-induced profound elevation of ROS and oxidative stress, as evidenced by the increase of lipid peroxidation level and the depletion of the total antioxidant capacity (TAC) level in the kidney, was suppressed by treatment with UA. UA also decreased 8-hydroxy-2-deoxyguanosine (one product of oxidative DNA damage) levels. Furthermore, protein expression by Western blot analysis showed that UA significantly decreased production of pro-inflammatory markers including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-17 (IL-17) and cyclooxygenase-2 (COX-2) in CCl4-treated mouse kidney. In exploring the underlying mechanisms of UA action, we found that UA increased the phosphorylation of transcription 3 (STAT3), which in turn activated the nuclear factor kappa B (NF-kappaB) and the inflammatory cytokines in the kidneys. In conclusion, these results suggested that the inhibition of CCl4-induced inflammation by UA is due at least in part to its anti-oxidant activity and its ability to modulate the STAT3 and NF-κB signaling pathways.

Protective role of cactus cladodes extract on sodium dichromate-induced testicular injury and oxidative stress in rats.

Cactus (Opuntia ficus-indica) is a xerophyte plant that belongs to the Cactaceae family. The present study was designed to investigate the possible protective effects of cactus cladodes extract (CCE) on sodium dichromate-induced testis damage in adult male Wistar rats. For this purpose, CCE at a dose of 100 mg/kg was orally administrated, followed by 10 mg/kg sodium dichromate (intraperitoneal injection). After 40 days of treatment, the rats were sacrificed, and the testes were excised for histological, lipid peroxidation (LPO), and antioxidant enzyme analyses. Sodium dichromate treatment significantly (P<0.01) decreased the body, testis, and accessory sex organ weights, sperm count and motility, and serum testosterone level. In addition, histological analysis revealed pronounced morphological alterations with tubular necrosis and reduction in the number of gametes in the lumen of the seminiferous tubules of sodium dichromate-intoxicated rats. Furthermore, exposure to sodium dichromate significantly (P<0.01) increased LPO level and decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in testis. Interestingly, pretreatment with CCE significantly (P<0.01) restored the serum testosterone level, sperm count, and motility to the levels of the control group. Moreover, CCE administration was capable of reducing the elevated level of LPO and significantly (P<0.01) increased SOD, CAT, and GPx activities in testis. Cactus cladodes supplementation minimized oxidative damage and reversed the impairment of spermatogenesis and testosterone production induced by sodium dichromate in the rat testis.

Tocopherol-deficient rice plants display increased sensitivity to photooxidative stress

Tocopherols are lipophilic antioxidants that are synthesized exclusively in photosynthetic organisms. Despite extensive in vivo characterization of tocopherol functions in plants, their functions in the monocot model plant, rice, remain to be determined. In this study, transgenic rice plants constitutively silenced for homogentisate phytyltransferase (HPT) and tocopherol cyclase (TC) activity were generated. Silencing of HPT and TC resulted in up to a 98 % reduction in foliar tocopherol content relative to the control plants, which was also confirmed by transcript level analysis. When grown under normal conditions, HPT and TC transgenics showed no distinctive phenotype relative to the control plants, except a slight reduction in plant height and a slight decrease in the first leaf length. However, when exposed to high light at low temperatures, HPT and TC transgenics had a significantly higher leaf yellowing index than the control plants. The tocopherol-deficient plants decreased their total individual chlorophyll levels, their chlorophyll a/b ratio, and the maximum photochemical efficiency of photosystem II, whereas increased lipid peroxidation levels relative to the control plants. Tocopherol deficiency had no effect on ascorbate biosynthesis, but induced glutathione, antheraxanthin, and particularly zeaxanthin biosynthesis for compensation under stressful conditions. However, despite these compensation mechanisms, HPT and TC transgenics still exhibited altered phenotypes under high light at low temperatures. Therefore, it is suggested that tocopherols cannot be replaced and play an indispensable role in photoprotection in rice.

Використання специфічних біомаркерів донних риб Керченської протоки для оцінки забруднення водних біоресурсів

The modern ecology situation in waters of the Kerch Strait requires assessment of disturbances in biotopes and monitoring of the degree of impact of industrial pollutants on ecosystem. Deposit of oil products after the 2007 year ships’ accidents might have considerable impact on the water biocenosis area. The investigation of cytoskeleton marker of astrocytes glial fibrillary acidic protein (GFAP) in brain of the bullhead (Neogobius fluviatilis), which is the typical representative of the commercial ground fish of the Kerch Strait, has been carried out. The results of comparative analysis of GFAP content in the brain of fish from the Kerch Bay near-shore waters and fish from conditionally clear area of Vorskla river shows the reliable (2.18 times) increasing of GFAP in the area of industrial pollution. Rising GFAP content indicates the astrogliosis development as a result of metabolic disturbances which can be induced by higher content of oil products in the near-bottom biotopes of the Kerch Bay. Increase in lipid peroxidation level was observed in the brain of fish from the Kerch Bay. The results provided with regard to violations of the state of astrocyte cytoskeleton and oxidative stress in the brain of bullhead from the Kerch Bay prove the sublethal biology effect of industrial pollutants in hydrobionts from this area. Results of this investigation also indicate the necessity of continuous ecology monitoring and comprehensive study of hydrobiont populations in the industrial regions and ecological disaster zones.

Effects of Temperature in Juvenile Seabass (Dicentrarchus labrax L.) Biomarker Responses and Behaviour: Implications for Environmental Monitoring

The effects of temperature on European seabass (Dicentrarchus labrax L.) juveniles were investigated using a 30-day bioassay carried out at 18 and 25 °C in laboratory conditions. A multiparameter approach was applied including fish swimming velocity and several biochemical parameters involved in important physiological functions. Fish exposed for four weeks to 25 °C showed a decreased swimming capacity, concomitant with increased oxidative stress (increased catalase and glutathione peroxidase activities) and damage (increased lipid peroxidation levels), increased activity of an enzyme involved in energy production through the aerobic pathway (isocitrate dehydrogenase) and increased activities of brain and muscle cholinesterases (neurotransmission) compared to fish kept at 18 °C. Globally, these findings indicate that basic functions, essential for juvenile seabass surviving and well performing in the wild, such as predation, predator avoidance, neurofunction and ability to face chemical stress may be compromised with increasing water temperature. This may be of particular concern if D. labrax recruitment phase in northwest European estuaries and coastal areas happens gradually in more warm environments as a consequence of global warming. Considering that the selected endpoints are generally applied in monitoring studies with different species, these findings also highlight the need of more research, including interdisciplinary and multiparameter approaches, on the impacts of temperature on marine species, and stress the importance of considering scenarios of temperature increase in environmental monitoring and in marine ecological risk assessment.

Bacterial lipopolysaccharide differently modulates steroidogenic enzymes gene expressions in the brain and testis in rats

Bacterial lipopolysaccharide (LPS) is a major component of the cell wall of gram negative bacteria contributing to the pathogenesis of bacterial infection, in particular in those diseases affecting central nervous system and reproductive tissues. The present work is an attempt to study the regulation of steroidogenic enzymes gene expression in the brain and testis in LPS induced rats. Adult male albino rats were administered LPS (5mg/kg BW) to induce acute inflammation. LPS administration induced severe oxidative damage in the brain and testicular tissue which was evident from decreased activities of enzymic antioxidants and increased lipid peroxidation levels. The mRNA expression of 3β-hydroxysteroid dehydrogenase (3β-HSD), 17β-hydroxysteroid dehydrogenase (17β-HSD) and androgen receptor corepressor-19kDa (ARR19) in the brain and testis were determined. The mRNA expression of 3β-HSD and 17β-HSD was increased in the brain with significant decrease in the testis at 24h and 48h in LPS treated animals. The results also demonstrated an interesting finding that LPS treatment completely represses ARR19 in the brain, while not in the testis. These findings show ARR19 might play a crucial role in regulation of neuronal and testicular steroidogenesis in inflammatory diseases.

Neuroprotection by the synthetic neurosteroid enantiomers ent-PREGS and ent-DHEAS against Aβ25–35 peptide-induced toxicity in vitro and in vivo in mice

Pregnenolone sulfate (PREGS) and dehydroepiandrosterone sulphate (DHEAS) are pro-amnesic, anti-amnesic and neuroprotective steroids in rodents. In Alzheimer's disease (AD) patient's brains, their low concentrations are correlated with high levels of Aβ and tau proteins. The unnatural enantiomer ent-PREGS enhanced memory in rodents. We investigated here whether ent-PREGS and ent-DHEAS could be neuroprotective in AD models. The effects of PREGS, ent-PREGS, DHEAS and ent-DHEAS against Aβ25-35 peptide-induced toxicity were examined in vitro on B104 neuroblastoma cells and in vivo in mice. B104 cells pretreated with the steroids before Aβ25-35 were analysed by flow cytometry measuring cell viability and death processes. Mice injected intracerebroventricularly with Aβ25-35 and the steroids were analysed for their memory abilities. Additionally, lipid peroxidation levels in the hippocampus were measured. ent-PREGS and PREGS significantly attenuated the Aβ25-35-induced decrease in cell viability. Both steroids prevented the Aβ25-35-induced increase in late apoptotic cells. PREGS further attenuated the ratio of necrotic cells. ent-DHEAS and DHEAS significantly reduced the Aβ25-35-induced toxicity and prevented the cells from entering late apoptosis and necrosis. All steroids stimulated neurite outgrowth per se and prevented the Aβ25-35-induced decrease. In vivo, ent-PREGS and ent-DHEAS significantly attenuated the Aβ25-35-induced decrease in memory (spontaneous alternation and passive avoidance) and an increase in lipid peroxidation levels. In contrast to the natural steroids, both enantiomers prevented amnesia when injected 6 h before Aβ25-35 in contrast to the natural steroids. The unnatural steroids ent-PREGS and ent-DHEAS are potent neuroprotective agents and could be effective therapeutical tools in AD.

Acute effect of aspartame-induced oxidative stress in Wistar albino rat brain.

The present study was carried out to investigate the acute effect of aspartame on oxidative stress in the Wistar albino rat brain. We sought to investigate whether acute administration of aspartame (75 mg/kg) could release methanol and induce oxidative stress in the rat brain 24 hours after administration. To mimic human methanol metabolism, methotrexate treated rats were used to study aspartame effects. Wistar strain male albino rats were administered with aspartame orally as a single dose and studied along with controls and methotrexate treated controls. Blood methanol and formate level were estimated after 24 hours and rats were sacrificed and free radical changes were observed in discrete regions by assessing the scavenging enzymes, reduce dglutathione (GSH), lipid peroxidation and protein thiol levels. There was a significant increase in lipid peroxidation levels, superoxide dismutase activity (SOD), glutathione peroxidase levels (GPx), and catalase activity (CAT) with a significant decrease in GSH and protein thiol. Aspartame exposure resulted in detectable methanol even after 24 hours. Methanol and its metabolites may be responsible for the generation of oxidative stress in brain regions. The observed alteration in aspartame fed animals may be due to its metabolite methanol and elevated formate. The elevated free radicals due to methanol induced oxidative stress.

Docosahexaenoic acid ameliorates aluminum induced biochemical and morphological alteration in rat cerebellum.

The omega-3 polyunsaturated fatty acids (PUFA), docosahexaenoic acid (DHA) have well-characterized effects on inflammation and oxidative stress and may have neuroprotective effects in a number of neurodegenerative conditions including AD. Brain tissue contains large amounts of polyunsaturated fatty acids, which are particularly vulnerable to free radical injury. The present study attempts to examine protective effects of docosahexaenoic acid (100 mg/kg body weight) and on aluminum (100 mg/kg b. wt. of AlCl3) mediated oxidative damage in the cerebellum in male albino rats along with the motor and learning ability and morphological changes. Twenty four male Rattusnorigious, Wistar strain rats (weight 220 ± 10 grams) were randomly divided into four groups (n = 12) viz. Group 1 served as control treated with normal saline, Group 2 treated with 100mg/kg body weight of DHA, Group three treated with 100 mg/kg body weight of AlCl3 and Group four treated with 100mg AlCl3 + 100 mg DHA for 90 days. Dose was directly introduced into the rat pharynx via a feeding cannula to rats for 90 days. Behavioral tests followed by biochemical analysis was performed. A significant decrease in the antioxidant status (superoxide dismutase, catalase, glutathione peroxidase and glutathione) and increased lipid peroxide levels and protein carbonyl content in aluminum exposed rats was noted. After DHA supplementation these effects were reversed. Moreover, DHA also significantly (p<0.05) prevented aluminum induced dysfunctioning of the motor and learning ability. The light microscopic studies revealed altered Purkinje's neurons and granular layer. These changes were not seen in the DHA treated rats. On the basis of our results it may be concluded that Al may be linked with cerebellar degeneration and neuromuscular disorders while DHA helps to prevent these alterations.

Protective Effect of Melatonin on Kainic Acid Induced-Liver Damage and Immune Modulatory Cytokines

Liver toxicity occurs when liver develops inflammation due to exposure to several toxic substances. The study was aimed to assess the liver damage induced by kainic acid and subsequently protective role of exogenous melatonin against the liver toxicity. Interestingly, kainic acid caused severe liver damage as evident from deleterious alterations in liver histology, increased lipid peroxide levels, decrease in the activities of liver anti-oxidant enzymes, DNA damage (adduct formation and sequence alterations), increased expression of cytokines like monocyte chemoattractant protein-1, interleukin 6, interferon γ and decreased expression of interleukin 10. These changes were normalized by melatonin (0.5-1.0 mM, (in vitro) or 10–20 mg/kg, (in vivo)). The study included assessment of the expression of immune modulatory cytokine mediators using real time PCR in both in vitro and in vivo conditions in the mouse liver. DNA damage was also studied. Various oxidative stress parameters and liver histopathology was also evaluated. Melatonin’s anti-kainic acid toxicity could be brought about by counter acting the influence of kainic acid on the levels of the cytokines, immune reactions and free radical production. This work suggests that melatonin receptors present could be mediate the hepatoprotective actions of melatonin therapy.

Protective effect of quercetin on atrazine-induced oxidative stress in the liver, kidney, brain, and heart of adult wistar rats.

Background:The conflicting roles of quercetin against tissue pathologies associated with oxidative stress are known.Objective:To evaluate the effect of quercetin at doses of 5 mg/kg (Q5) or 10 mg/kg (Q10) against atrazine (120 mg/kg, ATZ)-induced oxidative stress in various tissues of rats.Materials and Methods:Adult male albino Wistar rats were administered ATZ, Q5, and Q10 alone or in combination for 16 days. At the end of the 16th day, the animals were sacrificed by cervical dislocation; and the blood, heart, brain, kidney and liver were collected and used for biochemical determinations and histopathological examination.Results:Q10 but not Q5 attenuated ATZ-induced increase in the levels of serum enzyme markers sorbitol dehydrogenase (SDH), acid phosphatase (ACP), alkaline phosphatase (ALP), and aspartate aminotransferase (AST). The heart was less susceptible to ATZ-induced oxidative stress than the liver, kidney, and brain of treated animals, and there were tendencies for synergistic effects in the heart and liver of Q5 + ATZ-treated rats. Oxidative stress-induced by ATZ in terms of increased lipid peroxidation level and superoxide dismutase (SOD) activity was decreased in the brain of the Q5 + ATZ-treated rats but not that of the Q10 + ATZ-treated rats. Conversely, histopathological changes and oxidative stress-induced by ATZ in terms of elevated lipid peroxidation level, decreased SOD, and catalase (CAT) activities were prevented in the kidney and liver of the Q10 + ATZ-treated rats but not that of the Q5 + ATZ-treated rats.Conclusion:Quercetin at the investigated doses and especially the low dose may not protect against ATZ-induced oxidative stress in rat tissues in an overall sense.

Effects of 1,8-cineole on hypertension induced by chronic exposure to nicotine in rats

The monoterpenic oxide 1,8-cineole is a major component of many essential oils. We investigated its effects on systolic blood pressure (SBP) and oxidative stress in rats chronically exposed to nicotine. Male Sprague-Dawley rats (100-120 g) were intraperitoneally injected with 0.8 mg/kg/day nicotine for 21 days, followed by 3 mg/kg nicotine the next day. Rats were subsequently injected intraperitoneally with 0.01, 0.1 and 1 mg/kg 1,8-cineole, or 10 mg/kg nifedipine. SBP was measured using a tail cuff transducer, plasma nitrite concentration was measured colorimetrically, and plasma corticosterone concentration was measured by enzyme immunoassay. We found that 0.1 mg/kg 1,8-cineole significantly reduced SBP, and that 1.0 mg/kg 1,8-cineole significantly increased plasma nitrite concentrations, compared with rats chronically exposed to nicotine alone. Rats chronically exposed to nicotine showed a significant increase in lipid peroxidation levels, an elevation significantly antagonized by treatment with 0.01 mg/kg and 0.1 mg/kg 1,8-cineole. Chronic exposure to nicotine also significantly increased plasma corticosterone levels, but this effect was not diminished by treatment with 1,8-cineole. These results indicate that 1,8-cineole may lower blood pressure, and that this antihypertensive effect may be associated with the regulation of nitric oxide and oxidative stress in rats chronically exposed to nicotine.

Evaluation of in vitro toxicity of peptide (N-acetyl-Leu-Gly-Leu-COOH)-substituted-β-cyclodextrin derivative, a novel drug carrier, in PC-12 cells

BackgroundCyclodextrins (CDs) have been shown to improve physicochemical and biopharmaceutical properties of drugs when low solubility and low safety limit their use in the pharmaceutical field. Recently, a new amphiphilic peptide-substituted-β-CD, hepta-(N-acetyl-Leu-Gly-Leu)-β-CD (hepta-(N-acetyl-LGL)-β-CD), is developed which exhibited good solubility, strong inclusion ability and an appropriate average molecular weight. However, there is limited information available about its toxic effects. This study was designed to evaluate cytotoxic effects of the hepta-(N-acetyl-LGL)-β-CD (50, 200, 400, and 800 μg/ml) on rat pheochromocytoma PC-12 cells.ResultsA significant reduction of cell viability with IC50 values of 1115.0 μg/ml, 762.4 μg/ml, and 464.9 μg/ml at 6, 12, and 24 h post-treatment, respectively, as well as increased lipid peroxide levels and DNA damage were observed.ConclusionsIn conclusion, hepta-(N-acetyl-Leu-Gly-Leu)-β-CD exhibit significant toxic properties at high concentrations, probably through induction of oxidative stress and genotoxicity.

Effect of Atrazine, Glyphosate and Quinclorac on Biochemical Parameters, Lipid Peroxidation and Survival in Bullfrog Tadpoles (Lithobates catesbeianus)

Increased use of pesticides worldwide has led to damage not only to natural ecosystems but also to nontarget species. This study assessed the effects of different concentrations of the herbicides atrazine, glyphosate, and quinclorac on biochemical parameters, lipid peroxidation, and survival in tadpoles of Lithobates catesbeianus (bullfrog). Two hundred eighty-eight tadpoles were acquired from a frog farm in the south of Brazil. All animals were kept in aquariums under controlled laboratory conditions for 7days and exposed to commercial formulations of atrazine (5, 10, and 20μg/L), glyphosate (36, 72, and 144μg/L), and quinclorac (0.05, 0.10, and 0.20μg/L) for 7days thereafter. The concentrations used in this study are similar to the levels of these herbicides found in natural water bodies. After exposure, gill, liver, and muscle samples were removed from each animal for quantitation of glycogen, total lipids, triglycerides, cholesterol, total proteins, and lipid peroxidation. Atrazine, glyphosate, and quinclorac exposure induced a significant decrease in levels of glycogen and total lipids in gill, liver, and muscle. Triglycerides levels in the gill increased after exposure to glyphosate, and decreased after exposure to atrazine and quinclorac; their levels in liver and muscle decreased on exposure to all herbicides. Cholesterol and total protein levels decreased in liver and muscle for all three herbicides. All tissues exhibited increased lipid peroxidation after exposure to all herbicides. In conclusion, exposure to the herbicides tested in this study induced significant changes in biochemical parameters and increased lipid peroxidation levels in tadpoles of L. catesbeianus.

Zingerone regulates intestinal transit, attenuates behavioral and oxidative perturbations in irritable bowel disorder in rats

Stress can lead to the manifestation of functional gastrointestinal disorders, the most prominent being irritable bowel disorder. The present study investigated the impact zingerone in ameliorating chronic water stress induced irritable bowel disorder, brain gut axis dysfunction and dysregulation of the intestinal barrier due to oxidative stress. Rats were randomly allocated to groups and subjected to chronic water stress for a period of 21 days for 1h and the fecal pellet output was measured. At the end of chronic stress, behavioral assessment for anxiety like behavior was recorded and plasma corticosterone levels were measured 60min after water stress. The colonic transit was determined, levels of oxidative and antioxidant biomarkers were measured in the colon homogenate. Myeloperoxidase activity was determined as an indirect index of neutrophil infiltration. Chronic water stress increased the rate of colonic transit, fecal output, induced behavioral changes, and decreased antioxidant levels. An increase in lipid peroxide levels, catalase and corticosterone was observed. Mast cell infiltration was evident in the stressed group. Zingerone significantly reduced colonic transit, fecal output, neutrophil infiltration, and lipid peroxide formation. The levels of catalase were not altered; however, a marginal increase in the levels of glutathione peroxidase was observed. Zingerone significantly enhanced the levels of superoxide dismutase, glutathione and decreased the levels of corticosterone. Zingerone produced marked improvement in stress induced irritable bowel disorder which could be attributed to the powerful antioxidant nature, direct effect on the intestinal smooth muscle and adaptogenic nature.

PROTECTIVE EFFECT OF AQUEOUS EXTRACTS OF AFRAMOMUM MELEGUETA ON γ-RADIATION-INDUCED LIVER DAMAGE IN MALE WISTAR RATS

Summary This study was carried out to evaluate the radioprotective potential of aqueous extract of seeds of Aframomum melegueta (A.M.) against gamma radiation-induced (6Gy) liver damage in male Wistar rats. Thirty male rats were randomly distributed into six groups of five animals each and aqueous extract of A.M. was administered at a dose of 200 or 400 mg/kg b. wt., orally for 2 weeks prior to irradiation and 4 weeks after irradiation, when they were sacrificed. The hepatic antioxidant status; reduced glutathione (GSH), catalase (CAT) and glutathione peroxidase (GPx) as well as the extent of lipid peroxidation (LPO) were estimated. The activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined and histological examination was carried out. Exposure of animals to irradiation significantly increased LPO levels in comparison with the normal control group, reduced the level of GSH as well as CAT and GPx activity. On the other hand, there was a significant elevation in the activities of serum ALT and AST after irradiation exposure. Administration of aqueous extract of A.M. at a dose of 200 or 400 mg/kg before and after irradiation significantly decreased the elevated levels of LPO, restored GSH level near normal and enhanced CAT and GPx activities as well as significantly decreasing the elevated levels of serum ALT and AST activities. The histological examination and results from this study collectively indicate that aqueous extracts of A.M. could protect the liver from radiation-induced damage probably by enhancing the hepatic antioxidant defense mechanism in rats.

Protective effect of rutin on hexachlorobutadiene-induced nephrotoxicity

Hexachlorobutadiene (HCBD) is a potent nephrotoxin which nowadays contaminates human foods and water. On the other hands, it has been reported that rutin is a chemopreventive flavonoid which exerts some protective effects on the kidney. Therefore, in this work, the possible effect of rutin on HCBD-induced nephrotoxicity was investigated in female rats. The animals were divided into five groups. Groups 1 and 2 were treated with vehicle and HCBD (100 mg/kg, i.p.), respectively. Groups 3–5 were pretreated with rutin (100, 500 and 1000 mg/kg, i.p.) 1 h before HCBD injection. The level of serum urea and creatinine as well as urinary glucose and protein were measured. Total thiol content and lipid peroxidation level were also determined in the kidney homogenate. When compared to control group, a significant increase in the level of serum creatinine and urea (p < 0.001) as well as urine glucose and protein (p < 0.001) were observed after 24 h of HCBD administration. HCBD also caused a significant decrease in total thiol content (p < 0.001) and a significant increase in lipid peroxidation level (p < 0.001). Pretreatment with rutin could decrease serum creatinine (p < 0.001) and urea (p < 0.001) as well as urine protein (p < 0.001) concentrations when compared with HCBD treated rats. No significant modification on urine glucose was seen (p > 0.05). Rutin also reversed the HCBD-induced depletion in thiol content (p < 0.001) and elevation in lipid peroxidation (p < 0.001) in the kidney. The results of present study showed that rutin clearly attenuated HCBD-induced nephrotoxicity and has the potential to be considered as a nephroprotective agent.

Gastroprotective, cytoprotective and antioxidant effects of Oleum cinnamomi on ethanol induced damage

Peptic ulcer disease is a gastrointestinal disorder defined by mucosal damage and free oxygen radicals associated with peptic ulcer and gastritis. Cinnamon is a traditional herb used for many diseases and it has also effects as an antioxidant, anti-inflammatory, antispasmodic and anti-ulcerative. Our research is based on oxidative stress and effects of Oleum cinnamomi on stomach, liver and kidney disorders induced by ethanol. In our experiment, 2-3month old male Sprague-Dawley rats were used. One hour before the mucosal damage induced by 70% ethanol, O. cinnamomi (2.5ml/kg) was added into the groups. Gastric pH, analysis of gastric mucus and ulcer index were calculated from samples obtained from the stomach. Superoxide dismutase (SOD), malondialdehyde and catalase (CAT) levels were determined in stomach, liver and kidney homogenates and erythrocyte hemolysate. Histopathological examination of stomach, liver and kidney were determined with H&E staining. The non-treated ulcerative group showed higher scores than the control group which was treated with O. cinnamomi, when ulcer scores, gastric mucus and pH level of stomach are compared. Increased lipid peroxidation levels were observed in the liver, kidney and erythrocyte hemolysate. SOD activity was decreased in liver whereas increased in stomach of ethanol treated ulcerative groups. CAT levels were increased in stomach and liver of ethanol treated rats. Histopathological findings showed that ethanol treatment cause multiply organ damage such as stomach, liver and kidney injury. O. cinnamomi treatment protected these tissues from ethanol-induced damage. Consequently, the current investigation shows that O. cinnamomi has protective effects on ethanol-induced oxidative and mucosal damage.