Kidney Malondialdehyde Research Articles

The Influence of Gemfibrozil on Malondialdehyde Level and Paraoxonase 1 Activity in Wistar and Fisher Rats

There are diverse experimental data about the influence of gemfibrozil (GEM) on the production of hydrogen peroxide (H(2)O(2)) and antioxidant enzymes. We investigated the influence of GEM treatment on the production of malondialdehyde (MDA) level in tissues of normolipidaemic Wistar and Fisher rats which is an index of lipid peroxidation. Because serum paraoxonase 1 (PON1) is an important enzyme with specific protective function on metabolism of lipid peroxides, we examined the influence of GEM on PON1 activity in liver and serum. MDA level and enzyme activities were also determined 10 days after withdrawal of GEM treatment. The significantly increased levels of MDA in liver, kidney and heart of both rat strains were obtained after 3 weeks of GEM treatment. We propose two possibilities for the increase of MDA levels caused by GEM, induction of peroxisome proliferation and activities of enzymes that participated in occurrence of H(2)O(2) and possible reduction of enzyme activities including in H(2)O(2) metabolism. Ten days after withdrawal of GEM treatment, MDA levels in all tissue levels of both rat strains were less in comparison with GEM treatment. GEM caused a significant drop of PON1 activity in serum and liver of Fisher rats, and in liver of Wistar rats. We suggest that GEM, through induction of lipid peroxidation, caused the damage of hepatocytes with consequent reduction of PON1 synthesis. The increase in PON1 activity in serum and tissues of both rat strains 10 days after withdrawal of GEM treatment shows the fast recovery of enzyme synthesis.

The effect of N-acetyl cysteine on serum glutathione, TNF-α and tissue malondialdehyde levels in the treatment of sepsis

The aim of this study was to investigate the effects of Nacetyl cysteine (NAC) on the levels of reactive oxygen species in sepsis. In this study, 30 Sprague-Dawley female rats weighing 180- 200 g were used. Rats were randomized into three groups, each containing 10 rats, as follows: Group I: Sham, Group II: Sepsis and Group III: Sepsis+NAC. Group I underwent only laparotomy. In Groups II and III, sepsis was induced by cecal ligation and perforation (CLP) technique. NAC (20 mg/kg/ day) was administered orally to Group III at 0, 8 and 16 hours. At the 24th hour, tissue and blood samples were taken for erythrocyte glutathione (GSH) and serum tumor necrosis factor (TNF)-? levels, histopathological determination, and lung, liver and kidney tissue malondialdehyde (MDA) analyses. Group III was significantly different from the other groups with respect to erythrocyte glutathione, serum TNF-? and kidney MDA levels (p<0.05). There was no significant difference between the groups regarding liver MDA levels and histopathological parameters for lung, liver and kidney (p>0.05). NAC treatment had beneficial effects on erythrocyte GSH, serum TNF-?, lung function, and kidney MDA levels in sepsis-induced rats. However, this beneficial effect was not confirmed as histopathological improvement. Further research is needed to prove the effect of NAC in sepsis treatment.

Methanolic Extract of Cnidoscolus aconitifolius Attenuates Renal Dysfunction Induced by Chronic Ethanol Administration in Wistar Rats

The present work studied the modulatory role of methanolic extract of Cnidoscolus aconitifolius leaf (MECA) in rat model of renal dysfunction induced by chronic ethanol administration. Forty-two male Wistar albino rats weighing between 170 and 180 g were distributed into seven groups of six animals each. Some groups were pretreated with MECA (100 and 200 mg/kg) or kolaviron (KV) (200 mg/kg) for 2 weeks before simultaneous administration of MECA or KV and 20% ethanol (7.9 g/kg) for eight consecutive weeks. Others were given ethanol or MECA (200 mg/kg) or KV alone, and the control received corn oil (Vehicle). KV served as the standard antioxidant. In ethanol-treated rats, serum urea, creatinine, urinary glucose, gamma-glutamyltransferase and protein increased by 59, 81, 70, 148 and 63%, respectively, while creatinine clearance significantly (P < 0.05) decreased by 79%. MECA significantly (P < 0.05) attenuated the above biochemical indices to near normal. Also, the levels of serum and kidney malondialdehyde (MDA) (Index of lipid peroxidation) increased by 102 and 143%, respectively, in ethanol-treated rats. Ethanol intoxication caused a significant (P < 0.05) decrease in the levels of catalase (CAT), superoxide dismutase (SOD) and reduced glutathione (GSH) in kidney of the rats. MECA attenuated the ethanol-induced increases in serum and kidney MDA, and also enhanced the antioxidant status of the rats by increasing the levels of CAT, SOD and GSH. The activity of MECA was comparable with KV at 200 mg/kg. The biochemical findings were corroborated by histopathological examination of the kidney. The results suggest that the renal protective effect of C. aconitifolius leaf extract is by attenuating oxidative stress induced by chronic ethanol administration.

Nephrotoxicity induced by chromium (VI) in adult rats and their progeny

To assess kidney damages in pregnant and lactating rats and in their suckling pups, Wistar female rats were given, through drinking water, 700 parts per million (ppm) of K(2)Cr(2)O(7) from the 14th day of pregnancy until day 14 after delivery. Toxicity was objectified by a significant increase in malondialdehyde (MDA), glutathione (GSH) and nitric oxide (NO) levels in kidney of chromium-treated mothers and their suckling pups. Moreover, lactate dehydrogenase (LDH) was increased in kidney and decreased in plasma of K(2)Cr(2)O(7)-treated rats. Activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were increased in dams and decreased in their pups. Interestingly, these biochemical modifications were accompanied by higher plasma and lower urinary levels of creatinine, a specific indicator of glomerular function, and of urea than those of controls. Significant increase in creatinine clearance was also found in treated mothers and in their progeny. Histological studies showed an infiltration of mononuclear cells, necrosis and vascular congestion in kidney of pups and dams. Based on the present findings, K(2)Cr(2)O(7) administrated to female rats during late pregnancy and early postnatal periods provoked kidney damages in dams and their offspring.

Attenuation of cisplatin-induced nephrotoxicity in rats using zerumbone

Zerumbone is a natural compound isolated from the fresh rhizomes of Zingiber zerumbet. This bioactive compound has shown a chemo-preventive, anti-inflammatory and free radical scavenging activities. This study examines the effect of zerumbone on the extent of tissue damage in cisplatininduced nephrotoxicity in rats. The rats received a single dose injection of 10 mg/kg cisplatin. Other groups of rats received zerumbone (100 and 200 mg/kg), corn oil or the vehicle, dimethyl sulfoxide (DMSO) intraperitoneally for 4 days prior to cisplatin-injections. All animals were decapitated 16 h after cisplatin injection. Trunk blood was collected and analyzed for blood urea nitrogen (BUN) and serum creatinine. Kidney tissue was kept for the quantification of malondialdehyde and glutathione levels. Histopathological investigations were carried out and the severity of lesions was scored to obtain quantitative data. Our study revealed that zerumbone reduced kidney damage and preserved renal functions as proved by microscopic observations and lesion scoring. The increased in kidney malondialdehyde (MDA) levels with simultaneous glutathione (GSH) reduction in cisplatin treated group was attenuated by zerumbone (p < 0.05). It was concluded that zerumbone is beneficial in cisplatininduced renal dysfunction and organ damage in rats possibly via the prevention of lipid per oxidation and preservation of antioxidant glutathione.

Interactions of NADPH oxidase, renin–angiotensin–aldosterone system and reactive oxygen species in mequindox-mediated aldosterone secretion in Wistar rats

High doses of mequindox (MEQ) are associated with oxidative stress and pathological toxicity in the kidney. In this study, we demonstrated long term effects of MEQ on intra- or extra-adrenal renin–angiotensin–aldosterone system (RAAS) in vivo. RAAS plays a major role in aldosterone secretion. High doses of MEQ in the diet for 180 days in male rats led to inhibition of intra- and extra-adrenal RAAS, concident with down-regulation of Na +/K +-ATPase (NAKA) and mineralocorticoid receptor (MR), the downstream of aldosterone action. Significant changes of malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD) in kidney were also observed in the high doses (110, 275 mg/kg) groups. The mRNA levels of most subunits of NADPH oxidase were significantly upregulated at low doses (25–110 mg/kg) but the upregulation was diminished at higher doses in both kidney and adrenal gland, indicating a complicated and contradictory effect of MEQ on NADPH. These results highlight the complex interactions of drug metabolism, RAAS, NADPH oxidase and oxidative stress in response to MEQ-induced tissue toxicity and aldosterone secretion.

Protective effects of selenium on methimazole nephrotoxicity in adult rats and their offspring

This study aims to investigate the improving effects of selenium on methimazole-induced kidney impairments in adult rats and their pups. The animals were randomly divided into four groups of six each: group I served as control which received standard diet; group II received only methimazole in drinking water as 250 mg/l; group III received both methimazole (250 mg/l, orally) and selenium (0.5 mg/kg of diet); group IV served as a positive control and received selenium (0.5 mg/kg of diet) as sodium selenite (Na 2SeO 3). Treatments were started from the 14th day of pregnancy until day 14 after delivery. In the methimazole-treated group, body and absolute kidney weights decreased in pups and their mothers when compared to control. Daily urine volume, plasma creatinine levels were higher, while urinary levels were lower than in control. Besides, antioxidant enzyme activities, superoxide dismutase, catalase and glutathione peroxidase decreased. Lipid peroxidation recorded an increase revealed by high kidney malondialdehyde levels, while those of plasma and urinary uric acid showed a significant decline. Methimazole-treated rat kidneys exhibited leucocytic infiltrations, vascular congestion and narrowed Bowman's space. Co-administration of selenium through diet improved all the parameters cited above in adult rats and their progeny. Nevertheless, the distorted histoarchitecture in rat kidney was alleviated by selenium treatment. It can then be concluded that selenium is an important protective element that may be used as a dietary supplement against kidney impairments.

The protective effect of royal jelly against cisplatin-induced renal oxidative stress in rats

The aim of this study was to investigate the effects of royal jelly on cisplatin-induced nephrotoxicity and oxidative stress in rats. Adult male Wistar albino rats were randomly divided into eight groups: the control, cisplatin, royal jelly, and royal jelly plus cisplatin groups. Biochemical and histopathological methods were utilized for evaluation of the nephrotoxicity. Blood was collected and analyzed for blood urea nitrogen (BUN), alanine aminotransferase, aspartate aminotransferase, triglyceride, total cholesterol, uric acid, total bilirubin, and total protein levels. The kidney samples were stored for the measurement of malondialdehyde (MDA), glutathione peroxidase (GSHPx), superoxide dismutase (SOD), and catalase (CAT) activities and processed for histopathological examinations. Administration of cisplatin to rats induced a marked renal failure, characterized with a significant increase in serum BUN and uric acid concentrations, and they had higher kidney MDA and lower GSH-Px, SOD, and CAT activities. In the groups that were administered RJ in association with CP, improvement was observed in some oxidative stress parameters and certain other biochemical parameters, pre-treatment with RJ being more effective. The CP-induced changes in histopathologic findings of kidneys were partially reversed by treatment with royal jelly. The results provide further insight into the mechanisms of CP-induced nephrotoxicity and confirm the antioxidant potential of royal jelly.

Biochemical and Histological Changes in the Kidney of Streptozotocin‐Induced Diabetic Rats: Effects of Garlic and Ginger Compared to Aspirin

This study was conducted to determine the biochemical and histological efficacies of garlic and ginger in comparison to aspirin in streptozotocin‐induced diabetic rats. One week diabetic rats (blood glucose &gt; 300 mg/dl) were divided into four groups of which three groups were treated for 8 weeks with daily IP doses of fresh extracts of garlic and ginger (500 mg/kg each) or aspirin (10 mg/kg). Kidney malondialdehyde (MDA), lactate dehydrogenase (LDH), catalase (CAT), protein and total antioxidants were measured. The results showed that kidney MDA and LDH levels of diabetic non‐treated rats were significantly increased as compared to both the normal controls and the garlic‐, ginger‐ and aspirin‐treated animals. Total antioxidants levels of untreated diabetic rats were significantly lower than those of both the normal controls and the three treated groups. CAT and protein levels of untreated diabetic rats were significantly decreased as compared to the normal controls and the garlic‐ and ginger‐treated groups. Aspirin‐treated rats were not statistically different from the diabetic non‐treated rats in regard to CAT and protein and from the garlic‐ and ginger‐treated rats with respect to MDA and total antioxidants. Diabetic renal corpuscles showed general distortion, in particular deterioration in capsular membrane and reduction in capsular space. All treatments attenuated the renal corpuscle modulation with more potency exerted by garlic and ginger. Results suggest that the hypoglycaemic effects of garlic and ginger can help in ameliorating diabetic nephrology, and it is concluded that these two herbs can be administered as a supplementary precaution against diabetes.This work was partially supported by the College of Graduate Studies, Kuwait University.

Effect of calcitonin on lipid peroxidation in ovariectomized rats

Calcitonin is one of the active substances which is recently used effectively in osteoporosis treatment. In literature there is no information whether calcitonin cause oxidative stress or not. In this study, subcutaneous calcitonin is applied to rats having experimental postmenopausal osteoporosis and the effects of calcitonin on lipid peroxidation and antioxidant system were investigated. Forty-five healthy adult female Swiss albino Wistar rats were used in this study. The rats were divided into three equal groups as control, ovariectomized (Ovx) and ovariectomized+calcitonin (Ovx-CAL). The rats in Ovx and Ovx-CAL were anaesthetized and underwent a bilateral ovariectomy via ventral incision. Ten weeks after ovariectomy, salmon calcitonin (2 IU/kg body weight) was administered via s.c. at a volume of 1 mL per week for 12 weeks to the Ovx-CAL group. At the end of the drug treatment, livers and kidneys of rats were removed and malondialdehyde (MDA) levels and catalase (CAT) activities were determined by biochemical analysis methods. Data were analyzed by one-way ANOVA followed by the post-hoc LSD multiple test. The liver and kidney MDA levels were increased whereas the activity of CAT enzyme was decreased as a result of ovariectomy compared to values in the control group. Similar results were observed in Ovx-CAL group; however, the decline in the CAT activity in the kidney was not significant. In conclusion, we may suggest that calcitonin treatment increases the oxidative stress in osteoporotic rats.

Protective effect of N-acetylcysteine on experimental chronic lead nephrotoxicity in immature female rats

Oxidative stress plays a key role in lead (Pb)-induced nephrotoxicity. N-acetylcysteine (NAC) is a potent oxygen free radicals scavenger and a metal chelator. In the present study, female Sprague-Dawley rats received PbAc(2) (300 mg/L, via drinking water) and/or NAC (100 mg/kg/day, by intraperitoneal injection) to investigate the protective effect of NAC on Pb-induced renal damage and oxidative stress as well as its mechanism of action. Renal toxicity was evaluated by measuring urinary excretion of total protein, beta(2)-microglobulin, albumin and urinary enzyme markers of tubular necrosis, as well as serum urea nitrogen level. Activities of antioxidant enzymes, contents of glutathione and malondialdehyde in kidney were also measured. Renal cell damage was assessed by electron microscopy. Animals that received both Pb and NAC showed a better renal function than those receiving Pb alone. Lead-induced tubular lesions and mitochondrial damage were markedly reduced in rats that also received NAC. Also, NAC significantly reduced the levels of lipid peroxidation and markedly restored the enzymic and non-enzymatic antioxidants levels in kidney of Pb-treated rats. Moreover, NAC administration significantly increased urinary Pb excretion and decreased its level in the serum and kidney. In conclusion, NAC treatment prevents renal tubular damage induced by chronic Pb administration, most probably through its antioxidant properties and chelating ability.

Amelioration of cisplatin-induced nephrotoxicity by pravastatin in mice

This study investigated the protective effects of pravastatin against cisplatin-induced nephrotoxicity and the possible mechanisms in mice. Pravastatin showed significant protection as evidenced by the decrease of elevated serum creatinine (CRE) and blood urea nitrogen (BUN), and improvement of histopathological injury induced by cisplatin. The formation of kidney malondialdehyde (MDA) with a concomitant reduction of reduced glutathione (GSH) were inhibited by pravastatin, while the activities of kidney superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-px) were increased. The over expressions of kidney induced nitric oxide synthase (iNOS) and nitrotyrosine (3-NT) were suppressed by pravastatin. Pravastatin suppressed cisplatin-induced p38 mitogen-activated protein kinase (MAPK) activation in the kidney of mice. These results suggest that pravastatin pre-administration can prevent the nephrotoxicity induced by cisplatin. Pravastatin may exert the protective effect via inhibiting oxidative and nitrosative stress.

Protective effects of Forsythia suspensa extract against oxidative stress induced by diquat in rats

Forsythia suspensa extract has been proved as a potential antioxidant in the recent years. The present study was undertaken to obtain the optimal antioxidant fraction in vitro and examine its antioxidative potential against diquat-induced oxidative stress in male Sprague Dawley rats in vivo. In vitro, 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging experiment indicated that the CH 2Cl 2 fraction of F. suspensa (FSC) exerted the strongest scavenging activities; forsythoside A, forythialan A and phillygenin from it might be the major antioxidant constituents. In vivo, pretreatment of rats with different doses of FSC (25, 50 and 100 mg/kg bw) and vitamin C (100 mg/kg bw, positive control) for 15 days significantly lowered the tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in plasma compared to the negative control group. Also, FSC significantly increased the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and the levels of glutathione (GSH) in plasma, liver and kidney whereas it decreased the levels of malondialdehyde (MDA) in plasma and kidney. Moreover, the protective effect of FSC (100 mg/kg bw) was better than vitamin C. These results revealed that FSC exerted a protective effect against diquat-induced oxidative stress and is worthy of becoming a potential dietary antioxidant.

Cytotoxicity induced by alprazolam in rat vital organ

The current demonstrated the cytototoxic effects of alparazolam on the vital organs of rats. Animal were divided into two groups ; G1 : normal control (not received any drug), G2 : alpazolam treated group. The effects of this drug toxicity on different tissue vital organs tissues (liver,kidney and heart ) were studied after 10,20 and30 days from drug administration. The results revealed that administration of alprazolam induces oxidative tissue damage indicated by significant increase in the activity of xanthine oxidase (XO) with concomitant elevated level of nitric oxide(NO) in liver kidney and heart of alprazolam-treated rats in comparison with normal animals. The increment of such oxidative tissue damage markers was accompanied by increased malondialdehyde (MDA, index of lipid peroxidation) in kidney, and decrease in adenosine triphosphatatase (ATPase) and lactate dehdrogenase(LDH)activities in cardiac tissue. The oxidative tissue damage induced in liver in response to alprazolam ingestion was supported by a depletion in the activity of hepatic sobitol dehydrogenase(SD)copled with elevation in serum enzymes, aspirate aminotransferase (AST), alanine .

Protective effects of Selenium (Se) on Chromium (VI) induced nephrotoxicity in adult rats

Chromium is a toxic metal implicated in human diseases. This study was focused on investigating the possible protective effect of Se against K 2Cr 2O 7. Female Wistar rats, used in this study, were divided into four groups of six animals each: group I served as control which received standard diet; group II received orally only K 2Cr 2O 7 (700 ppm equivalent to 67 mg/kg bw); group III received both K 2Cr 2O 7 and Se (0.5 mg/kg of diet); group IV received Se (0.5 mg Na 2SeO 3/kg of diet). The exposure of rats to K 2Cr 2O 7 for 21 days provoked renal damages with a significant increase in kidney malondialdehyde, superoxide dismutase, plasma creatinine, and uric acid levels, while catalase, glutathione peroxidase, non-protein thiol, Metallothionein and plasma urea levels decreased. Coadministration of Se in the diet of chromium-treated group improved malondialdehyde, renal biomarkers levels and antioxidant enzyme activities. Kidney histological studies confirmed biochemical parameters and the beneficial role of selenium.

Effect of 3-(1H-Pyrrol-2-yl)-1H-Indazole on the Antioxidant Status of Rats

The influence of injection periods of 3-(1H-pyrrol-2-yl)-1H-indazole regarding vitamins A, E, C, selenium (Se), malondialdehyde (MDA) levels, and glutathione peroxidase (GSH-Px) activity in rats has been investigated. The substance was given by subcutaneous injection at 20 mg/kg every other day for a total of 15 injections. At the end of the treatment, Se levels in serum were determined by fluorimetry, and those of vitamins A, E, C, and malondialdehyde in serum, liver, and kidney were determined by high-performance liquid chromatography. GSH-Px activities in erythrocytes were determined spectrophotometrically. Vitamins A, E, C, and Se levels were generally lower than in the controls, while GSH-Px activity at the third injection period was maximally increased, with the activities after the other injection periods being higher than in the control group. In addition, vitamins A, E, and C levels were generally lower than the control groups, while serum, liver, and kidney MDA levels gradually increased depending on injection periods. On the other hand, GSH-Px activity was higher than in the control group. Thus, the results show that while vitamins A, E, C, and Se levels decreased, MDA levels and GSH-Px activities increased after administration of 3-(1H-pyrrol-2-yl)-1H-indazole to the rats. These findings might be related to the increased amount of free radicals caused by 3-(1H-pyrrol-2-yl)-1H-indazole injection.

Vitamin alleviates visceral lipid peroxidative injury in dogs during oral fluid resuscitation of burn shock

To investigate the effect of vitamin C (VC) on visceral lipid oxidative injury during oral fluid resuscitation of burn shock. Twelve male Beagle dogs were surgically prepared for arterial and venous cannulation, and 24 hours later they were subjected to a 50% TBSA full-thickness flame injury. In the first 24 hours after burn dogs were resuscitated with gastric infusion of either glucose-electrolyte solution (GES group, n = 6) or GES containing 250 mg/kg of VC (GES/VC group, n = 6). The delivery rate and volume of GES was in accordance with that of Parkland formula (4 ml x kg(-1) x 1% TBSA(-1) in the first 24 hours). In the second 24 hours all animals received delayed i.v. fluid resuscitation. At end of 72 hours after injury, animals were sacrificed, and specimens of heart, lung, liver, kidney and jejunum were harvested for evaluation of xanthine oxidase (XOD), malondialdehyde (MDA) and assessment of the tissue water content (ratio of dry to wet weight) of organs. The plasma levels of alanine aminotransferase (ALT), creatinine (Cr), MB isoenzyme of creatine kinase (CK-MB) and diamine oxidase (DAO) were determined at same time. At 72 hours after burn it was showed significant higher activities of XOD in GES/CAR than GES group in heart, kidney and jejunum, and lower contents of MDA in heart, lung, liver, kidney and jejunum (P all < 0.01). Tissue water contents were significantly lower in GES/CAR than GES group in heart [(75.4 +/-1.1)% vs (78.5 +/- 0.8)%], lung [(68.1 +/- 0.9)% vs (73.9 +/- 1.0)%], liver [ (75.2 +/- 0.8)% vs (78.3 +/- 1.2)%], kidney [(73.8 +/- 1.1)% vs (78.1 +/- 0.8)%] and jejunum [(76.3 +/- 0.8)% vs ( 80.4 +/- 0.6)] respectively, all P < 0.01. The levels of ALT, CK-MB, Cr and DAO in GES/CAR group were (46.6 +/- 2.49) U/L, (43.4 +/- 7.05) mol/L, (7156 +/- 596) U/L and (1.86 +/- 0.45) U/L respectively, all significantly lower than those of the GES group [(86.9 +/- 7.89) U/L, (95.2 +/- 1.23) mol/L, (8023 +/- 384) U/L and (2.68 +/- 0.61) U/L respectively, all P < 0.05]. The results indicated that vitamin C alleviated visceral tissue edema and organ injury by inhibiting free radical production during oral fluid resuscitation of burn shock.

Toxic effects of lambda-cyhalothrin, a synthetic pyrethroid pesticide, on the rat kidney: Involvement of oxidative stress and protective role of ascorbic acid

Lambda-cyhalothrin is a synthetic pyrethroid insecticide used worldwide in agriculture, home pest control, protection of foodstuff and disease vector control. The objective of this study was to investigate the propensity of lambda-cyhalothrin (LTC) to induce oxidative stress, changes in biochemical parameters and enzyme activities in the kidney of male rats and its possible attenuation by Vitamin C (vit C). Renal function, histopathology, tissue malondialdehyde (MDA), protein carbonyl (PCO) levels, antioxidant enzyme activities and reduced glutathione (GSH) levels were evaluated. Exposure of rats to lambda-cyhalothrin, during 3 weeks, caused a significant increase in kidney MDA and protein carbonyl levels ( p<0.01) as compared to controls. Co-administration of vitamin C was effective in reducing MDA and PCO levels. The kidney of LTC-treated rats exhibited severe vacuolations, cells infiltration and widened tubular lumen. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione- S-transferase (GST) were significantly decreased due to lambda-cyhalothrin exposure. Co-administration of vitamin C ameliorated the increase in enzymatic activities of aminotransferases (AST and ALT), lactate dehydrogenase (LDH), creatinine and urea levels and improved the antioxidant status. These data indicated the protective role of ascorbic acid against lambda-cyhalothrin-induced nephrotoxicity and suggested a significant contribution of its antioxidant property to these beneficial effects.

Quorum sensing is necessary for the virulence of Pseudomonas aeruginosa during urinary tract infection

Quorum sensing is a signaling pathway used by bacteria to monitor their population density by detecting small diffusible molecules. To understand the role of quorum sensing in pathogenesis of urinary tract infections, wild type Pseudomonas aeruginosa, having both functional las and rhl quorum sensing systems, and its isogenic single and double mutants were used in a mouse model of ascending urinary tract infection. Mice were evaluated on the basis of bacteriological and histopathological examinations, detection of acyl homoserine lactone, and the pathologic index factors of renal and bladder tissue. Single as well as double mutant strains were able to reach renal tissue, but they were not able to multiply and cause tissue damage. Reduced rates of infection, mild histopathologic lesions, and decreased production of pathologic index factors like myeloperoxidase, malondialdehyde, and reactive nitrogen intermediates were found in these groups of mice as compared to mice infected with a standard strain (PAO1) possessing both functional sensing systems. Loss of any one of the quorum-sensing components significantly reduced the in vivo virulence of P. aeruginosa in this mouse model of ascending urinary tract infection. Our results suggests that quorum-sensing signals may act as virulence factors and are essential for P. aeruginosa multiplication and virulence during the course of urinary tract infection.

Melatonin and 1400 W Ameliorate both Intestinal and Remote Organ Injury Following Mesenteric Ischemia/Reperfusion

Acute intestinal ischemia reperfusion (I/R) injury affects not only the intestines but also remote organs due to pro-inflammatory and tissue injurious factors. Thus, we aimed to investigate the roles of melatonin (a powerful antioxidant) and 1400W (a strong inhibitor of inducible nitric oxide) in a rat intestinal I/R injury model, since oxidative and nitrosative injury are believed to be the major causes. A total of 56 Wistar albino rats were used, with seven rats in each group. After I/R induction in the intestines by clamping/unclamping the superior mesenteric artery, we measured malondialdehyde, superoxide dismutase, glutathione peroxidase, nitric oxide, and 3-nitrotyrosine levels in lung, kidney, and liver tissues (to evaluate remote organ injury) as well as in the intestines. Study groups received melatonin, 1400W or both to examine the roles of these molecules in the pathogenesis of injury following I/R. Melatonin and 1400W had an ameliorating effect on both oxidative and nitrosative stress in the intestine and the lung against mesenteric I/R injury in rats. Moreover, each of these two agents had an inhibitory effect on oxidative injury and histopathological changes in the intestine and the lung. Furthermore, the combination of both agents (melatonin and 1400W) was more effective than either of the agents alone (P < 0.05). Melatonin and 1400W, either alone or in combination, were efficient in ameliorating experimental I/R injury of the intestines.