Rosmarinus officinalis essential oil modulates renal toxicity and oxidative stress induced by potassium dichromate in rats

BACKGROUNDChromium hexavalent (CrVI) is known as a toxic contaminant that induced oxidative stress and nephrotoxicity in humans and animals. Rosmarinus officinalis is a perennial herb rich in biologically active constituents that have powerful antioxidant properties. So, the current work evaluated the effectiveness of Rosmarinus officinalis essential oil (REO) against alterations induced by potassium dichromate in the kidney of male rats.METHODSGC-MS analysis, in vitro total phenol contents, and DPPH scavenging activity of REO were estimated. Thirty-five Wistar male rats were categorized into 5 groups. The first group was the control, the second one was orally administered rosemary essential oil (REO; 0.5 mL/kg BW), the third group was injected intraperitoneally with hexavalent chromium (CrVI; 2 mg/kg BW) for 14 days, the fourth group used as the protective group (REO was administrated 30 min before i.p. injection of CrVI) and the fifth group applied as the therapeutic group (rats injected with CrVI 30 min followed by oral administration of REO), respectively.RESULTSTwenty-nine components were detected with high total phenolic contents and high DPPH scavenging activity. Results revealed that CrVI- intoxicated rats showed a valuable increase in oxidative stress profile (TBARS and H₂O₂) and a notable decline in glutathione (GSH), total protein content, and enzymatic antioxidants (SOD, CAT, GPx, and GST). Furthermore, serum kidney functions biomarkers (urea, creatinine, and uric acid) were increased significantly. Also, the administration of CrVI showed histological and immunohistochemical (PCNA-ir) changes in rat kidney tissue. Otherwise, administration of REO pre or post-treatment with CrVI significantly restored most of the biochemical parameters in addition to improvement in kidney tissue architecture. Moreover, individual intake with REO exhibited an amendment in oxidative stress markers.CONCLUSIONConclusively, REO had a potential antioxidant capacity in ameliorating K₂Cr₂O₇-induced nephrotoxicity, especially in the protection group.     

Metformin and silymarin afford protection in cyclosporine A induced hepatorenal toxicity in rat by modulating redox status and inflammation

The use of cyclosporine A (CsA) as an immunosuppressive agent is often limited owing to its hepatotoxic and nephrotoxic properties. The present study was designed to evaluate the protective effect of metformin and silymarin in a rat model of CsA induced hepatorenal toxicity. The study included seven groups of Wistar albino rats (n = 6 per group): normal control, experimental control (CsA alone, 25 mg/kg), CsA + metformin (50 and 500 mg/kg), CsA + silymarin (50 and 200 mg/kg) and CsA + vitamin E (100 mg/kg). All the drugs were given daily for a period of 21 days by oral gavage and their effect was evaluated on serum levels of organ function markers (serum glutamate pyruvate transaminase, serum glutamate oxaloacetate transaminase, bilirubin, urea/blood urea nitrogen, creatinine), markers of oxidative stress (thiobarbituric acid reactive substances, glutathione, superoxide dismutase), inflammation (nitrite, myeloperoxidase, tumour necrosis factor‐alpha, prostaglandin E₂), apoptosis (terminal deoxynucleotidyl transferase dUTP nick end labelling positivity) in addition to tissue histology, cyclooxygenase (COX)‐2 and inducible nitric oxide synthase (iNOS) immunoreactivity. Administration of metformin and silymarin along with CsA ameliorated functional damage to liver and kidneys in a dose‐dependent manner. Significant and comparable improvement in the tissue levels of oxidative stress, inflammation, apoptotic markers was also observed following treatment with both the test drugs. Normalization of histology scores, as well as COX‐2 and iNOS immunoreactivity scores, further strengthened these findings. The hepatoprotective and nephroprotective effects of metformin and silymarin were comparable and matched with that of reference drug, vitamin E. The findings of the present study suggest that both metformin and silymarin have a potential for clinical use in patients receiving long‐term CsA treatment to maintain their liver and kidney functions.     

Antioxidant therapy for management of oxidative stress induced hypertension

Hypertension is considered as the most common risk factor for cardiovascular diseases, also is regarded as a leading cause of the mortality and morbidity worldwide. The mechanisms underlying the pathological process of hypertension are not completely explained. However, there is growing evidence that increased oxidative stress plays an important role in the pathophysiology of hypertension. Several preclinical studies and clinical trials have indicated that antioxidant therapy is important for management of hypertension, using antioxidants compounds such as alpha tocopherol (Vit E) and ascorbic acid (Vit C), polyphenols with others and some antihypertensive drugs that are now in clinical use (e.g. ACEIs, ARBs, novel B-blockers, dihydropyridine CCBs) which have antioxidative pleiotropic effects. The purpose of this review is to highlight the importance of antioxidant therapy for management of oxidative stress induced hypertension. Furthermore, we review the current knowledge in the oxidative stress and its significance in hypertension.     

Protective effects of vitexin on cadmium-induced renal toxicity in rats

Cadmium (Cd) is an industrial contaminant that poses severe threats to human and animal health. Vitexin (VIT) is a polyphenolic flavonoid of characteristic pharmacological properties. We explored the curative role of vitexin on Cd-induced mitochondrial-dysfunction in rat renal tissues. Twenty-four rats were equally divided into four groups and designated as control, Cd, Cd + vitexin and vitexin treated groups. The results showed that Cd exposure increased urea and creatinine levels while decreased creatinine clearance. Cd reduced the activities of antioxidant enzymes, i.e., catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione content in the Cd exposed group. Cd exposure significantly (p < 0.05) elevated the reactive oxygen species (ROS) and Thiobarbituric acid reactive substances (TBARS) levels in rat kidney. Cd also caused a significant (p < 0.05) reduction in the mitochondrial TCA-cycle enzymes, including isocitrate dehydrogenase, succinate dehydrogenase, alpha-ketoglutarate dehydrogenase, and malate-dehydrogenase activities. Besides, mitochondrial respiratory chain enzymes, including NADH-dehydrogenase, coenzyme Q-cytochrome reductase, succinic-coenzyme Q, and cytochrome c-oxidase activities were also decreased under Cd exposure. Cd exposure also damaged the mitochondrial membrane potential (MMP). However, VIT treatment potentially reduced the detrimental effects of Cd in the kidney of rats. In conclusion, our study indicated that the VIT could attenuate the Cd-induced renal toxicity in rats.     

An insect model for assessing oxidative stress related to arsenic toxicity

The potential usefulness of an insect model to evaluate oxidative stress induced by environmental pollutants was examined with trivalent arsenic (As³⁺, NaAsO₂) and pentavalent arsenic (As⁵⁺, Na₂HAsO₄) in adult female house flies, Musca domestica, and fourth-instar cabbage loopers, Trichoplusia ni. M. domestica was highly susceptible to both forms of arsenic following 48 h exposure in the drinking water with LC₅₀s of 0.008 and 0.011% w/v for As³⁺ and As⁵⁺, respectively. T. ni larvae were susceptible to dietary As³⁺ with an LC₅₀ of 0.032% w/w but seem to tolerate As⁵⁺ well with an LC₅₀ of 0.794% concentration after 48 h exposure. The minimally acute LC₅ dose of both As³⁺ and As⁵⁺ varied considerably but averaged 0.005% for both insects. The potential of both valencies of arsenic for inducing oxidative stress in the insects exposed ad libitum to approximately LC₅ levels was assessed. The parameters examined were the alterations of the antioxidant enzyme activities of superoxide dismutase (SOD), catalase (CAT), glutathione transferase (GST), the peroxidase activity of glutathione transferase (GSTPX), and glutathione reductase (GR), and increases in lipid peroxidation and protein oxidation. SOD (1.3-fold), GST (1.6-fold), and GR (1.5-fold) were induced by As³⁺ in M. domestica but CAT and GSTPX were not affected. As⁵⁺ had no effect on M. domestica. In T. ni, the antioxidant enzyme activities were not affected by As³⁺ except for SOD which was suppressed by 29.4% and GST which was induced by 1.4-fold. As⁵⁺ had no effect except the suppression of SOD by 41.2%. Lipid peroxidation and protein oxidation, which represent stronger indices of oxidative stress, were elevated in both insects by up to 2.9-fold. However, based on the antioxidant enzyme response to the arsenic anions, the mode of action of arsenic induced oxidative stress may differ between the two insects. Until this aspect is further clarified, evidence at this time favors the prospect of As³⁺ as a pro-oxidant, especially for M. domestica. © 1995 Wiley-Liss, Inc.     

Melatonin attenuates methotrexate‐induced oxidative stress and renal damage in rats

Nephrotoxicity is an adverse side effect of methotrexate (MTX) chemotherapy. The present study verifies whether melatonin, an endogenous antioxidant prevents MTX‐induced renal damage. Adult rats were administered 7 mg/kg body weight MTX intraperitoneally for 3 days. In the melatonin pretreated rats, 40 mg/ kg body weight melatonin was administered daily intraperitoneally 1 h before the administration of MTX. The rats were killed 12 h after the final dose of MTX/vehicle. The kidneys were used for light microscopic and biochemical studies. The markers of oxidative stress were measured along with the activities of the antioxidant enzymes and myeloperoxidase activity in the kidney homogenates. Pretreatment with melatonin reduced MTX induced renal damage both histologically and biochemically as revealed by normal plasma creatinine levels. Melatonin pretreatment reduced MTX induced oxidative stress, alteration in the activity of antioxidant enzymes as well as elevation in myeloperoxidase activity. The results suggest that melatonin has the potential to reduce MTX induced oxidative stress, neutrophil infiltration as well as renal damage. As melatonin is an endogenous antioxidant and is non‐toxic even in high doses it is suggested that melatonin may be beneficial in minimizing MTX induced renal damage in humans. Copyright © 2010 John Wiley & Sons, Ltd.     

Protective effect of proanthocyanidins against doxorubicin‐induced nephrotoxicity in rats

Doxorubicin (DOX) exerts toxic effects in several organs particularly kidney. The present study aimed to assess the protective effect of proanthocyanidins (PAs) against DOX‐induced nephrotoxicity in rats. A single dose of DOX (7.5 mg/kg, i.v.) significantly increased kidney weight, kidney/body weight ratio, serum urea, creatinine, tumor necrosis factor alpha levels, and kidney contents of malondialdehyde, nitric oxide, cyclooxygenase‐2, and caspase‐3 activity with significant reduction in final body weight, serum albumin, kidney contents of reduced glutathione (GSH), and superoxide dismutase activity as compared with control group. In contrast, pretreatment with PAs (200 mg/kg, p.o.) for 14 days before DOX and for 7 days after DOX ameliorated kidney function and oxidative stress parameters. Histopathological evidence confirmed the protective effects of PAs from the tissue damage induced by DOX. In conclusion, PAs have a multi‐nephroprotective effect that might be attributed to its antioxidant, anti‐inflammatory, and antiapoptoic activities.     

Effect of Emblica officinalis (Gaertn) on CCl4 induced hepatic toxicity and DNA synthesis in Wistar rats

A single dose of CCl4 (1 ml/kg body weight, po in corn oil) increased the levels of SGOT (serum glutamate oxaloacetate transaminase), SGPT (serum glutamate pyruvate transaminase), LDH (lactate dehydrogenase), glutathione-S-transferase and depletion in reduced glutathione, glutathione peroxidase and glutathione reductase. It also caused enhancement in the levels of lipid peroxidation (LPO) and DNA synthesis. There was also pathological deterioration of hepatic tissue as evident from multivacuolated hepatocytes containing fat globules around central vein. The pretreatment of E. officinalis for 7 consecutive days showed a profound pathological protection to liver cell as depicted by univacuolated hepatocytes. Pretreatment with E. officinalis at doses of 100 and 200 mg/kg body weight, prior to CCl4 intoxication showed significant reduction in the levels of SGOT, SGPT, LDH, glutathione-S-transferase, LPO and DNA synthesis. There was also increase in reduced glutathione, glutathione peroxidase and glutathione reductase. The results suggest that E. officinalis inhibits hepatic toxicity in Wistar rats.     

Magnitude of Hyperoxic Stress and Degree of Lung Maturity Determine the Nature of Pulmonary Antioxidant Response in the Guinea Pig

The ability of the immature lung to induce antioxidant defences in response to hyperoxic stress was examined. Preterm guinea pigs (65 days gestation, term = 68 d) were exposed to either 21+ O2, 85+ O2 or 95+ O2 for 72 hours. Exposure to 85+ O2 increased lung catalase, glutathione peroxidase and manganese superoxide dismutase activities in comparison to air controls. Exposure to 95+ O2 resulted only in an increase in glutathione peroxidase activity. Bronchoalveolar lavage fluid GSH concentration was increased by a similar amount by both exposure regimes, while lung copper/zinc superoxide dismutase activity was unchanged by either treatment. Comparison of the antioxidant response of term and preterm animals exposed to 85+ O2 for 72 hours indicated a greater response in the lung of the preterm animals. Manganese superoxide dismutase activity was elevated in both term and preterm animals, while catalase and glutathione peroxidase activities were elevated only in preterm animals. The extent of microvascular permeability as indicated by bronchoalveolar lavage fluid protein concentration, was lower in preterm animals than in term animals. We conclude that the immature lung can respond to hyperoxic stress by antioxidant induction and that the nature of the response is dependent, in part, both on the severity of the stress and on the maturity of the lung.     

Magnitude of Hyperoxic Stress and Degree of Lung Maturity Determine the Nature of Pulmonary Antioxidant Response in the Guinea Pig

The ability of the immature lung to induce antioxidant defences in response to hyperoxic stress was examined. Preterm guinea pigs (65 days gestation, term = 68 d) were exposed to either 21+ O2, 85+ O2 or 95+ O2 for 72 hours. Exposure to 85+ O2 increased lung catalase, glutathione peroxidase and manganese superoxide dismutase activities in comparison to air controls. Exposure to 95+ O2 resulted only in an increase in glutathione peroxidase activity. Bronchoalveolar lavage fluid GSH concentration was increased by a similar amount by both exposure regimes, while lung copper/zinc superoxide dismutase activity was unchanged by either treatment. Comparison of the antioxidant response of term and preterm animals exposed to 85+ O2 for 72 hours indicated a greater response in the lung of the preterm animals. Manganese superoxide dismutase activity was elevated in both term and preterm animals, while catalase and glutathione peroxidase activities were elevated only in preterm animals. The extent of microvascular permeability as indicated by bronchoalveolar lavage fluid protein concentration, was lower in preterm animals than in term animals. We conclude that the immature lung can respond to hyperoxic stress by antioxidant induction and that the nature of the response is dependent, in part, both on the severity of the stress and on the maturity of the lung.     

Acute toxicity and adverse effects of aqueous and ethanol extracts of Parkia biglobosa pods on biochemical parameters of Clarias gariepinus

The acute toxicity of the aqueous and ethanol extracts of Parkia biglobosa pods against Clarias gariepinus was investigated under laboratory conditions. Agitated behaviours and respiratory distress were also observed during the exposure period. The adverse effects on biochemical parameters were assessed using semi-static bioassays for 28 days. The ethanol extract of P. biglobosa pods was found to be more acutely toxic with a 96 h LC₅₀ value of 13.96 mg l^?1 than the aqueous extracts, with a 96 h LC₅₀ value of 19.95 mg l^?1 against C. gariepinus. Both extracts induced agitated behaviours and respiratory distress in exposed organisms. The activities of superoxide dismutase (SOD), catalase (CAT) and the concentration of malondialdehyde (MDA) were significantly lower (p < 0.05) in groups of organisms exposed to extracts of P. biglobosa when compared with the control group after 14 days. The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were also significantly (p < 0.05) lower compared with activities of the enzymes in the control group after 28 days. The current study has shown that the introduction of P. biglobosa pods into aquatic ecosystems is acutely toxic to fish and would possibly be to other non-target aquatic organisms especially invertebrates.     

Restorative effects of Chrysin pretreatment on oxidant–antioxidant status,inflammatory cytokine production,and apoptotic and autophagic markers in acute paracetamol‐induced hepatotoxicity in rats: An experimental and biochemical study

Paracetamol (PC) is a widely used analgesic and antipyretic drug, but it leads to acute hepatotoxicity at high doses intakes. This study was aimed to investigate the effects of Chrysin (CR) on hepatotoxicity constituted at high doses of PC in rats. Rats were subjected to oral pretreatment of CR (25 and 50 mg/kg b.w.) via feeding needle for 6 days against hepatotoxicity induced by a single dose of PC (500 mg/kg b.w.) administered orally via feeding needles. Although PC increases lipid peroxidation and liver enzyme activities, it has led to reduction of antioxidant enzyme activities. PC induced inflammatory responses by increasing the levels of TNF‐α and IL‐1β. Furthermore, PC caused apoptosis and autophagy by increasing activity of Caspase‐3 and LC3B level. On the other hand, CR therapy significantly regulated these values in rats. This study demonstrated that CR possesses restorative effect against PC‐induced hepatotoxicity by suppressing oxidative stress, inflammation, and apoptotic and autophagic tissue damage.     

Antioxidant responses to water deficit by drought‐tolerant and ‐sensitive sugarcane varieties

Water deficit is the major yield‐limiting factor of crop plants. The exposure of plants to this abiotic stress can result in oxidative damage due to the overproduction of reactive oxygen species. The aim of this work was to study the antioxidant‐stress response of drought‐tolerant (SP83‐2847 and SP83‐5073) and drought‐sensitive (SP90‐3414 and SP90‐1638) sugarcane varieties to water‐deficit stress, which was imposed by withholding irrigation for 3, 10 and 20 days. The drought‐sensitive varieties exhibited the lowest leaf relative water content and highest lipid peroxidation, hydrogen peroxide (H₂O₂) and proline contents during the progression of the drought‐stress condition. The antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), guaiacol peroxidase (GPOX) and glutathione reductase (GR) activities changed according to variety and stress intensity. SP83‐2847 exhibited higher CAT and APX activities than the other varieties in the early stage of drought, while the activities of GPOX and GR were the highest in the other varieties at the end of the drought‐stress period. A Cu/Zn SOD isoenzyme was absent at the end of drought period from the SP90‐3414‐sensitive variety. The results indicate that lipid peroxidation and early accumulation of proline may be good biochemical markers of drought sensitivity in sugarcane.     

Effect of bioactive tannoid principles of Emblica officinalis on iron-induced hepatic toxicity in rats.

The tannoid principles of the fruits of the plant Emblica officinalis Gaertn comprising of emblicanin A. emblicanin B, punigluconin and pedunculagin, have been reported to exhibit antioxidant activity in vitro and in vivo. In the present study, an emblicanin A (37%) and B (33%) enriched fraction of fresh juice of Emblica fruits (EOT), administered prophylactically (10, 20 and 50 mg/kg, p.o.) for 10 consecutive day, was found to inhibit acute iron overload (30 mg/kg, i.p.) hepatic lipid peroxidation and the increase of serum levels of alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase, used as markers of the induced hepatic dysfunction. A similar effect was produced by silymarin (20 mg/kg, p.o.), an antioxidant hepatoprotective agent. The results support the use of Emblica fruits for hepatoprotection in Ayurveda.     

Thyroid Hormone Influences Antioxidant Defense System in Adult Rat Brain

The objective of the current study was to find out whether thyroid hormone influences antioxidant defense parameters of rat brain. Several oxidative stress and antioxidant defense parameters of mitochondrial (MF) and post-mitochondrial (PMF) fractions of cerebral cortex (CC) of adult rats were compared among euthyroid (control), hypothyroid [6-n-propylthiouracil (PTU)-challenged], and hyperthyroid (T3-treatment to PTU-challenged rats) states. Oxidative stress parameters, such as thiobarbituric acid-reactive substances (TBA-RS) and protein carbonyl content (PC), in MF declined following PTU challenge in comparison to euthyroid rats. On the other hand, when PTU-challenged rats were treated with T3, a significant increase in the level of oxidative stress parameters in MF was recorded. Hydrogen peroxide content of MF as well as PMF of CC was elevated by PTU-challenge and brought to normal level by subsequent treatment of T3. Although mitochondrial glutathione (reduced or oxidized) status did not change following PTU challenge, a significant reduction in oxidized glutathione (GSSG) level was noticed in PMF following the treatment. T3 administration to PTU-challenged rats had no effect on mitochondrial glutathione status. Total and CN-resistant superoxide dismutase (SOD) activities in MF of CC augmented following PTU challenge. CN-resistant SOD activity did not change when PTU-challenged rats were treated with T3. Although CN-sensitive SOD activity of PMF remained unaltered in response to PTU challenge, its activity increased when PTU-challenged rats were treated with T3. Catalase activity in PMF of CC of PTU-challenged rats increased, whereas the activity was decreased when hypothyroid rats were treated with T3. Similarly, total and Se-dependent glutathione peroxidase (GPx) activities of MF increased following PTU challenge and reduced following administration of T3. Se-independent GPx activity of MF and PMF and glutathione reductase activity of PMF decreased following PTU challenge and did not change further when rats were treated with T3. On the other hand, glutathione S-transferase activity of MF and PMF of CC did not change following PTU challenge but decreased below detectable level following T3 treatment. Results of the current investigation suggest that antioxidant defense parameters of adult rat brain are considerably influenced by thyroid states of the body.     

Protective effects of ascorbic acid on hepatotoxicity and oxidative stress caused by carbon tetrachloride in the liver of Wistar rats

This study was planned to investigate the protective effect of l (+)‐ascorbic acid (Vit C) on CCl₄‐induced hepatotoxicity and oxidative stress in the liver of Wistar rats (Rattus Norvegicus, strain Wistar). Twenty‐four adult male Wistar rats were fed with standard rat chow diet for 10 days and randomly were divided into four groups of six each as follows: (1) control, (2) CCl₄, (3) “CCl₄ + Vit C”, (4) Vit C groups. CCl₄ was applied to rats belonging to CCl₄ and “CCl₄ + Vit C” groups subcutaneously at 1 mg kg^?1 dose CCl₄ for 3 days. Vit C applied to “CCl₄ + Vit C” and “Vit C” group rats intraperitoneally at 300 mg kg^?1 dose for 3 days. All rats were sacrificed and livers were quickly removed on the fourth day of the experiment. MDA, total glutathione (T.GSH) levels and superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH‐PX) activities were measured in the liver of all groups of rats and also serum alanine amino transferase (ALT) and aspartate amino transferase (AST) activities were detected to determine liver functions in all groups of rats. Histopathological changes were evaluated by light and transmission electron microscopes. In “CCl₄ + Vit C” group, MDA level was significantly decreased (p < 0.05) and SOD, CAT, GSH‐PX activities were significantly increased (p < 0.005, 0.01, 0.05) respectively, T.GSH level was significantly increased (p < 0.005) and serum ALT and AST activities were significantly decreased (p < 0.01, 0.05), respectively, when compared with CCl₄ group. These results show that Vit C has a highly protective effect on hepatotoxicity and oxidative stress caused by CCl₄. Copyright © 2009 John Wiley & Sons, Ltd.     

Cardioprotective properties of natural medicine in isoproterenol induced myocardial damage in the male Albino rats

The main aim of this study is to investigate cardioprotective properties of natural medicine inmyocardial damage induced male Albino rats. The aqueous extractof Allium sativumwas used for the determination of phenolic compounds and flavonoids. The amount of phenol (1.39 ± 0.37 GAE/g dry weight) and flavonoids (49.1 ± 2.79 QE/g dry weight) were high in aqueous extract. A. sativumextract and showed 68.39 ± 3.6% DPPHscavenging activity. Isoproterenol was used to induce myocardial injury in Albino rats in vivo by subcutaneous injection (100 mg/kg body weight). To achieve this, experimental animals were categorized into six groups (n = 4), namely, positive, negative control, only isoproterenol administered groups, and garlic extract administered group at 100–300 mg extract/kg body weight. Oxidative stress marker and cardiac markers were assayed to analyze the cardioprotective properties of garlic extract. At 300 mg/kg doseof garlic extract, rat was recovered from various altered factors such as, aspartate aminotransferase, alkaline transminase and alkaline phosphatase. The rats treated with 300 mggarlic extract/kg body weight decreased the level of asparate aminotransferase (126 ± 6.4 IU/L) than other lower doses (100 mg extract/kg and 200 mg extract/kg). Alkaline transaminase level of rat serum level was 81 ± 4.34 IU/L. In the isoproterenol treated rats elevated level was observed (152 ± 4.42 IU/L enzyme activity). Pre-treatment of Albino rat with A. sativum extract reduced cardiac damage. Isoproterenol exposed animal showed 207.6 ± 1.2 mg/dL triglyceride and the garlic administered rat (300 mgextract/kg) reduced LDL-cholesterol level (61.3 ± 1.3 mg/dL) significantly (p < 0.05). Creatinine kinase -MB level was 269.5 ± 12.5 IU/L in the control animal and stress induced animal showed elevated level (572.3 ± 19.4 IU/L). Garlic treated experimental animal (300 µg/kg bw) decreased CK-MB level. To conclude, the aqueous extract of A. sativumshowed cardio protective properties against myocardial injury.     

Oxidative stress induced by lead, cadmium and arsenic mixtures: 30-day, 90-day, and 180-day drinking water studies in rats: An overview

Humans are frequently exposed to combinations of lead (Pb), cadmium (Cd) and Arsenic (As) but there is a paucity of actual data on the molecular effects of these agents at low dose levels. The present factorial design studies were undertaken in rats to examine the effects of these agents at LOEL dose levels on a number of molecular parameters of oxidative stress in hematopoietic and renal organ systems following oral exposure in drinking water at 30, 90 and 180 day time points. Results of these studies demonstrated dynamic, time-dependent alterations in both molecular targets and inducible oxidative stress protective systems in target cell populations. In general, cellular protective systems, which protected against oxidative damage at the 90 day time point, appeared to be finite such that molecular manifestations of oxidative stress became statistically significant at the 180 day time point for several of the combination exposure groups. These data demonstrate the importance of duration of exposure in assessing the toxic potential of Pb, Cd and As mixtures at low dose levels.     

Has vitamin E any shreds of evidence in cisplatin‐induced toxicity

Cisplatin is one of the highly consumed and effective antitumor agents whose clinical application is accompanied by nephrotoxicity adverse reaction. Also, other complications such as ototoxicity and hepatotoxicity are a matter of concern. Today, it is suggested that cisplatin‐associated toxicities are mainly induced by free radicals production, which will result in oxidative organ injury. The evidence is growing over the protective effects of antioxidants on cisplatin‐induced adverse reactions especially nephrotoxicity. The possible protective effects of vitamin E and its derivative in cisplatin‐induced nephrotoxicity and ototoxicity are reviewed here at the light of pertinent results from basic and clinical research. Administration of vitamin E alone or in combination with other antioxidant agents could cause amelioration in oxidative stress biomarkers such as decreasing the level of malondialdehyde, reducing serum urea and creatinine, and also enhancing the activities of renal antioxidant enzymes including renal catalase, glutathione‐S‐transferase, and superoxide dismutase. Although the data from most of the studies are in favors of protective effects of vitamin E against cisplatin‐induced toxicity, more clinical trials are needed to clarify the clinical importance of vitamin E administration as an antioxidant during cisplatin therapy in cancer condition.     

Influence of kolaviron and vitamin E on ethylene glycol monoethyl ether‐induced haematotoxicity and renal apoptosis in rats

The present study investigated the protective effects of kolaviron, a biflavonoid from the seed of Garcinia kola, and vitamin E on ethylene glycol monoethyl ether (EGEE)‐induced haematotoxicity and renal apoptosis in male rats. EGEE was administered at a dose of 200 mg kg^?1 alone or simultaneously administered with kolaviron (100 and 200 mg kg^?1) and vitamin E (50 mg kg^?1) for 14 days. Results of haematological examination showed that white blood cells, platelets, neutrophils and mean corpuscular haemoglobin concentration were significantly lower, whereas lymphocytes were increased in EGEE‐exposed rats compared with those in the control. Administration of EGEE caused a significant decrease in the superoxide dismutase and catalase activities as well as in the glutathione level but significantly increased glutathione Stransferase activity and levels of hydrogen peroxide and lipid peroxidation in kidneys of rats compared with those in the control. Also, EGEE‐treated rats showed significant elevation in the serum urea and creatinine with marked increase in the frequency of terminal deoxynucleotidyl transferase‐mediated dUTP nick end labelling assay‐positive apoptotic cells in the tubular epithelial cells in comparison with the control. Co‐administration with kolaviron or vitamin E exhibited chemoprotective effects against EGEE‐mediated haematotoxicity, augmented renal antioxidant status and prevented the induction of renal apoptosis. Copyright © 2013 John Wiley & Sons, Ltd.