Vitamin E and Hippophea rhamnoides L. extract reduce nicotine‐induced oxidative stress in rat heart

The effects of vitamin E and Hippophea rhamnoides L. extract (HRe‐1) on nicotine‐induced oxidative stress in rat heart were investigated. There were eight rats per group and supplementation period was 3 weeks. The groups were: nicotine [0.5 mg kg^?1day^?1, intraperitoneal (i.p.)]; nicotine plus vitamin E [75 mg kg^?1day^?1, intragastric (i.g.)]; nicotine plus HRe‐1 (250 mg kg^?1day^?1, i.g.); and the control group (receiving only vehicles). Nicotine increased the malondialdehyde level, which was prevented by both vitamin E and HRe‐1. Glutathione peroxidase (GPx) activity in nicotine plus vitamin E supplemented group was higher than the others. Glutathione S‐transferase (GST) activity in nicotine plus HRe‐1 supplemented group was increased compared with the control group. Catalase activity was higher in nicotine group compared with others. GPx activity in nicotine plus vitamin E supplemented group was elevated compared with the others. Total and non‐enzymatic superoxide scavenger activities in nicotine plus vitamin E supplemented group were lower than nicotine plus HRe‐1 supplemented group. Superoxide dismutase (SOD) activity was higher in nicotine plus HRe‐1 supplemented group compared with others. Glutathione reductase activity and nitric oxide level were not affected. Increased SOD and GST activities might have taken part in the prevention of nicotine‐induced oxidative stress in HRe‐1 supplemented group in rat heart. Flavonols such as quercetin, and isorahmnetin, tocopherols such as α‐tocopherol and β‐tocopherol and carotenoids such as α‐carotene and β‐carotene, reported to be present in H. rhamnoides L. extracts may be responsible for the antioxidant effects of this plant extract. Copyright © 2010 John Wiley & Sons, Ltd.     

The effects of vitamins and selenium mixture against brain tissue induced by d‐galactosamine

Brain damage is a major complication of fulminant hepatic failure. d ‐Galactosamine (d ‐GalN)‐induced liver toxicity causes damage to brain. The effects of vitamins and selenium mixture against d ‐GalN stimulated brain injury were investigated in this study. Sprague‐Dawley female rats aged 2.0‐2.5 months were used for the study. The rats were divided into four categories. A 0.9% NaCl solution was intraperitoneally given to the experimental rats in the first group. Using gavage technique, the second group of animals were subjected to a formulation consisting of 100 mg·kg^?1·day^?1 vitamin C, 15 mg·kg^?1·day^?1 of β‐carotene, 100 mg·kg^?1·day^?1 of α‐tocopherol in addition to 0.2 mg·kg^?1·day^?1 of sodium selenate for 3 days. The third group was given a single dose of d ‐GalN hydrochloride at the concentration of 500 mg·kg^?1 through a saline injection. The final group was given similar concentrations of both the antioxidant combination and d ‐GalN. Tissue samples were collected under ether anesthesia. The rats treated with d ‐GalN showed brain damage; increased myeloperoxidase, catalase, glutathione peroxidase, glutathione‐S‐transferase, lactate dehydrogenase, and superoxide dismutase activities; and decreased glutathione levels. Treatment with vitamins and selenium combination resulted in alleviation of these alterations in the rats. These findings suggest that administration of the vitamins and selenium combination suppresses oxidative stress and protects brain cells from injury induced by d ‐GalN.     

Protective effects of antioxidant combination against D‐galactosamine‐induced kidney injury in rats

The protective effects of an antioxidant combination in kidney injury induced by the injection of D‐galactosamine (D‐GaIN) were examined in the present study. Sprague Dawley female rats were used and divided into four groups as follows: (1) animals injected physiological saline solution, intraperitoneally, (2) animals treated with the combination of ascorbic acid (100 mg kg^?1 day^?1), β‐carotene (15 mg kg^?1 day^?1), α‐tocopherol (100 mg kg^?1 day^?1), and sodium selenate (0.2 mg kg^?1 day^?1) for three days orally, (3) rats injected D‐GaIN (500 mg kg^?1) intraperitoneally as a single dose, and (4) animals treated with the antioxidant combination for three days, then injected D‐GaIN. The tissue and blood samples of animals were collected for morphological and biochemical evaluations. Histopathological injury in kidney tissues was observed together with a significant increase in tissue lipid peroxidation (LPO) level, myeloperoxidase (MPO), lactate dehydrogenase, catalase and superoxide dismutase (SOD) activities, and serum creatinine and urea levels, and a significant decrease in glutathione level and glutathione peroxidase activity in D‐GaIN injected rats. However, a decrease in the degenerative changes was detected in the kidney tissue of D‐GaIN + antioxidant group, and biochemical results showed reversed effects. In conclusion, it seems reasonable to conclude that the treatment of the antioxidant combination has a protective effect on D‐GaIN‐induced kidney injury of rats. Copyright © 2010 John Wiley & Sons, Ltd.     

Kolaviron,a biflavonoid complex of Garcinia kola seeds modulates apoptosis by suppressing oxidative stress and inflammation in diabetes-induced nephrotoxic rats

Diabetic nephropathy is a complex disease that involves increased production of free radicals which is a strong stimulus for the release of pro-inflammatory factors. We evaluated the renal protective effect of kolaviron (KV) – a Garcinia kola seed extract containing a mixture of 5 flavonoids, in diabetes-induced nephrotoxic rats. Male Wistar rats were divided into 4 groups: untreated controls (C); normal rats treated with kolaviron (C + KV); untreated diabetic rats (D); kolaviron treated diabetic rats (D + KV). A single intraperitoneal injection of streptozotocin (STZ, 50 mg/kg) was used for the induction of diabetes. Renal function parameters were estimated in a clinical chemistry analyzer. Markers of oxidative stress in the kidney homogenate were analyzed in a Multiskan Spectrum plate reader and Bio-plex Promagnetic bead-based assays was used for the analysis of inflammatory markers. The effect of kolaviron on diabetes-induced apoptosis was assessed by TUNEL assay. In the diabetic rats, alterations in antioxidant defenses such as an increase in lipid peroxidation, glutathione peroxidase (GPX) activity and a decrease in catalase (CAT) activity, glutathione (GSH) levels and oxygen radical absorbance capacity (ORAC) were observed. There was no difference in superoxide dismutase (SOD) activity. Diabetes induction increased apoptotic cell death and the levels of interleukin (IL)-1β and tumor necrosis factor (TNF)-α with no effect on IL-10. Kolaviron treatment of diabetic rats restored the activities of antioxidant enzymes, reduced lipid peroxidation and increased ORAC and GSH concentration in renal tissues. Kolaviron treatment of diabetic rats also suppressed renal IL-1β. The beneficial effects of kolaviron on diabetes-induced kidney injury may be due to its inhibitory action on oxidative stress, IL-1β production and apoptosis.     

Hesperidin regresses cardiac hypertrophy by virtue of PPAR‐γ agonistic,anti‐inflammatory,antiapoptotic, and antioxidant properties

Hesperidin (HES), a flavanone glycoside, predominant in citrus fruits, has an agonistic activity on peroxisome proliferator‐activated receptor gamma (PPAR‐γ). PPAR‐γ is an inhibitor of cardiac hypertrophy (CH) signaling pathways. In this study, we investigated the cardioprotective effect of HES in isoproterenol (ISO)‐induced CH through PPAR‐γ agonistic activity. For this, male albino Wistar rats were divided into six groups (n = 6), that is, normal, ISO‐control, HES treatment group (200 mg kg^?1; p.o.), HES per se (200 mg kg^?1; p.o.), enalapril treatment group (30 mg kg^?1; p.o.), and combination group (HES 200 mg kg^?1; p.o.+enalapril 30 mg kg^?1; p.o.). ISO (3 mg kg^?1; s.c.) was administered to all groups except normal and per se to induce CH. HES or enalapril treatment of 28 days significantly attenuated pathological changes, improved cardiac hemodynamics, suppressed oxidative stress, and apoptosis along with an increased PPAR‐γ expression. The combination of enalapril with HES exhibited an effect similar to that of HES or enalapril alone on all the aforementioned parameters. Therefore, HES may be further evaluated as a promising molecule for the alleviation of CH.     

Caffeic acid phenethyl ester changes the indices of oxidative stress in serum of rats with renal ischaemia–reperfusion injury

Oxygen‐derived free radicals have been implicated in the pathogenesis of renal injury after ischaemia–reperfusion. Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, exhibits antioxidant properties. To investigate whether treatment with either CAPE or alpha‐tocopherol modifies the levels of the endogenous indices of oxidant stress, we examined their effects on an in vivo model of renal ischaemia–reperfusion injury in rats. CAPE at 10 μmol kg^?1 or alpha‐tocopherol at 10 mg kg^?1 was administered intraperitoneally before reperfusion. Acute administration of both CAPE and alpha‐tocopherol altered the indices of oxidative stress differently in renal ischaemia–reperfusion injury. Copyright © 2001 John Wiley & Sons, Ltd.     

Methylmercury toxicity: amelioration by selenium and water‐soluble chelators as N‐acetyl cysteine and dithiothreitol

The protective potential of chelators, i.e. N‐acetyl cysteine (0.6 mg /kg, intraperitoneally) and dithiothreitol (15.4 mg kg^?1, intraperitoneally) with selenium (0.5 mg kg^?1, pre‐oral) were evaluated individually and in combination against methylmercury‐induced biochemical alterations and oxidative stress consequences. Forty‐two male Sprague–Dawley rats were exposed with methylmercury (1.5 mg kg^?1, pre‐oral) daily for 21 days followed by different treatments for five consecutive days. Administration of methylmercury caused significant enhancement in the release of transaminases, alkaline phosphatases and lactate dehydrogenases in serum. A significant increased was observed in lipid peroxidation level with a concomitant decreased in glutathione content after methylmercury exposure in liver, kidney and brain. Hepatic microsomal drug metabolizing enzymes (aniline hydroxylase and amidopyrine N‐demethylase) of cytochrome p4502E₁ showed sharp depletion after methylmercury exposure. Alterations in histological changes in liver, kidney and brain were also noted in methylmercury administered group. All treated groups showed recovery pattern, but the combined treatments with N‐acetyl cysteine and dithiothreitol in combination with selenium were more effective than that with either alone treatments in recovering blood biochemical changes after methylmercury toxicity. In conclusion, the results demonstrated that combination therapy may recover all blood biochemical alterations and offer maximum protection against methylmercury‐induced toxicity. Copyright © 2014 John Wiley & Sons, Ltd.     

Silibinin ameliorates arsenic induced nephrotoxicity by abrogation of oxidative stress, inflammation and apoptosis in rats

Arsenic (As) is an environmental and industrial pollutant that affects various organs in human and experimental animals. Silibinin is a naturally occurring plant bioflavonoid found in the milk thistle of Silybum marianum, which has been reported to have a wide range of pharmacological properties. A body of evidence has accumulated implicating the free radical generation with subsequent oxidative stress in the biochemical and molecular mechanisms of As toxicity. Since kidney is the critical target organ of chronic As toxicity, we carried out this study to investigate the effects of silibinin on As-induced toxicity in the kidney of rats. In experimental rats, oral administration of sodium arsenite [NaAsO₂, 5?mg/(kg?day)] for 4?weeks significantly induced renal damage which was evident from the increased levels of serum urea, uric acid, creatinine with a significant (p?<?0.05) decrease in creatinine clearance. As also significantly decreased the levels of urea, uric acid and creatinine in urine. A markedly increased levels of lipid peroxidation markers (thiobarbituric acid reactive substances and lipid hydroperoxides) and protein carbonyl contents with significant (p?<?0.05) decrease in non-enzymatic antioxidants (total sulfhydryl groups, reduced glutathione, vitamin C and vitamin E) and enzymatic antioxidants (superoxide dismutase, catalase, glutathione peroxidase and glutathione S-transferase), Glutathione metabolizing enzymes (glutathione reductase and glutathione-6-phosphate dehydrogenase) and membrane bound ATPases were also observed in As treated rats. Co-administration of silibinin (75?mg/kg?day) along with As resulted in a reversal of As-induced biochemical changes in kidney accompanied by a significant decrease in lipid peroxidation and an increase in the level of renal antioxidant defense system. The histopathological and immunohistochemical studies in the kidney of rats also shows that silibinin (75?mg/kg?day) markedly reduced the toxicity of As and preserved the normal histological architecture of the renal tissue, inhibited the caspase-3 mediated tubular cell apoptosis and decreased the NADPH oxidase, iNOS and NF-κB over expression by As and upregulated the Nrf2 expression in the renal tissue. The present study suggests that the nephroprotective potential of silibinin in As toxicity might be due to its antioxidant and metal chelating properties, which could be useful for achieving optimum effects in As-induced renal damage.     

Effects of varying levels of dietary vitamin E (α‐tocopherol) on growth performance,proximate and fatty acid composition of juvenile silver pomfret (Pampus argenteus Euphrasen, 1788)

This study investigated the effects of elevated dietary levels of vitamin E (α‐tocopherol) on growth performance, proximate composition and fatty acid profiles of juvenile silver pomfret, Pampus argenteus. Three semi‐purified experimental diets were formulated to contain 49% protein and 16% lipid. High docosahexaenoic acid (DHA) tuna oil was added to the diets to supplement DHA. A graded level of vitamin E (0‐, 50‐, and 100 mg kg^?1) was added to experimental diets 1 to 3, respectively. Analyzed vit. E levels were 155.2, 195.3 and 236.4 mg kg^?1 in diets 1, 2 and 3, respectively. The experiment was conducted for 12 weeks with juvenile silver pomfret (29.6 ± 7.6 g) using a flow‐through system consisting of nine 1‐m³ tanks. Each treatment had three replicates and fish were stocked at the rate of 20 m^?3. Growth performance and feed utilization parameters of fish fed diets 2 and 3 were significantly (P < 0.05) higher than in fish fed diet 1, but the parameters in diets 2 and 3 did not differ significantly (P > 0.05). Although whole body protein levels were not influenced by the dietary vit. E levels, whole body lipid in fish fed diet 2 was significantly higher than in fish fed the other diets. The whole body vit. E levels in fish fed diet 2 (22.6 mg kg^?1) and diet 3 (24.1 mg kg^?1) were significantly (P < 0.05) higher than in those fed diet 1 (18.2 mg kg^?1). Whole body total saturated fatty acids were significantly lower, and DHA levels higher in fish fed diets 2 and 3 than those fed diet 1. The results of the present study suggest that increasing dietary supplementation of vit. E in high lipid diets enhances the growth performance of fish and that a dietary level of 196 mg kg^?1 vit. E is suitable for the growth of silver pomfret.     

Lactating and nonlactating rats differ to renal toxicity induced by mercuric chloride: the preventive effect of zinc chloride

This study evaluated the effects of HgCl₂ on renal parameters in nonlactating and lactating rats and their pups, as well as the preventive role of ZnCl₂. Rats received 27 mg kg^?1 ZnCl₂ for five consecutive days and 5 mg kg^?1 HgCl₂ for five subsequent days (s.c.). A decrease in δ‐aminolevulinic acid dehydratase (δ‐ALA‐D) activity in the blood and an increase in urine protein content in renal weight as well as in blood and urine Hg levels were observed in lactating and nonlactating rats from Sal―Hg and Zn―Hg groups. ZnCl₂ prevented partially the δ‐ALA‐D inhibition and the proteinuria in nonlactating rats. Renal Hg levels were increased in all HgCl₂ groups, and the ZnCl₂ exposure potentiated this effect in lactating rats. Nonlactating rats exposed to HgCl₂ exhibited an increase in plasma urea and creatinine levels, δ‐ALA‐D activity inhibition and histopathological alterations (necrosis, atrophic tubules and collagen deposition) in the kidneys. ZnCl₂ exposure prevented the biochemical alterations. Hg‐exposed pups showed lower body and renal weight and an increase in the renal Hg levels. In conclusion, mercury‐induced nephrotoxicity differs considerably between lactating and nonlactating rats. Moreover, prior exposure with ZnCl₂ may provide protection to individuals who get exposed to mercury occupationally or accidentally. Copyright © 2014 John Wiley & Sons, Ltd.     

Dietary vitamin A requirement of juvenile Amur sturgeon (Acipenser schrenckii)

The present experiment was conducted to determine the dietary vitamin A requirement of juvenile Amur sturgeon (Acipenser schrenckii) by formulating seven semipurified diets containing 10, 258, 510, 1050, 2020, 4100 and 8300 IU vitamin A (as retinol acetate) kg^?1 diet, respectively. Each experimental diet was fed to triplicate groups of 20 juveniles each with initial average weights of 12.09 ± 0.22 g in 405‐L aquaria and maintained at 25.0 ± 2.0°C for 8 weeks. Fish fed the basal diet (10 IU vitamin A kg^?1 diet) exhibited poor appetite and activity, whereas these signs were not observed in any group fed vitamin A‐supplemented diets. Weight gain, feed efficiency and hepatosomatic index increased significantly with increases in the dietary vitamin A level, reaching a peak with the vitamin A 1050 IU kg^?1 diet, and then decreasing. Muscle chemical compositions were not affected by the dietary vitamin A levels. Vitamin A concentrations in liver and muscle increased significantly as the vitamin A levels increased within a range of 10～4100 IU kg^?1 diet; above this level there were no significant changes. Broken‐line regression analysis of weight gain and liver vitamin A concentration against the dietary vitamin A level showed that juvenile Amur sturgeon required a minimum of 923 IU vitamin A kg^?1 in the diet for maximal growth, and 1981 IU kg^?1 for highest liver vitamin A accumulation.     

L‐NAME co‐treatment prevent oxidative damage in the lung of adult Wistar rats treated with vitamin A supplementation

Based on the fact that vitamin A in clinical doses is a potent pro‐oxidant agent to the lungs, we investigated here the role of nitric oxide (NO^?) in the disturbances affecting the lung redox environment in vitamin A‐treated rats (retinol palmitate, doses of 1000–9000 IU·kg^?1·day^?1) for 28 days. Lung mitochondrial function and redox parameters, such as lipid peroxidation, protein carbonylation and the level of 3‐nytrotyrosine, were quantified. We observed, for the first time, that vitamin A supplementation increases the levels of 3‐nytrotyrosine in rat lung mitochondria. To determine whether nitric oxide (NO ?) or its derivatives such as peroxynitrite (ONOO‐) was involved in this damage, animals were co‐treated with the nitric oxide synthase inhibitor L‐NAME (30 mg·kg^?1, four times a week), and we analysed if this treatment prevented (or minimized) the biochemical disturbances resulting from vitamin A supplementation. We observed that L‐NAME inhibited some effects caused by vitamin A supplementation. Nonetheless, L‐NAME was not able to reverse completely the negative effects triggered by vitamin A supplementation, indicating that other factors rather than only NO? or ONOO‐ exert a prominent role in mediating the redox effects in the lung of rats that received vitamin A supplementation. Copyright © 2011 John Wiley & Sons, Ltd.     

Carbofuran Induced Oxidative Stress Mediated Alterations in Na+‐K+‐ATPase Activity in Rat Brain: Amelioration by Vitamin E

Pesticides cause oxidative stress and adversely influence Na⁺‐K⁺‐ATPase activity in animals. Since impact of carbofuran has not been properly studied in the mammalian brain, the ability of carbofuran to induce oxidative stress and modulation in Na⁺‐K⁺‐ATPase activity and its amelioration by vitamin E was performed. The rats divided into six groups received two different doses of carbofuran (15% and 30% LD₅₀) for 15 days. The results suggested that the carbofuran treatment caused a significant elevation in levels of malonaldehyde and reduced glutathione and sharp inhibition in the activities of super oxide dismutase, catalase, and glutathione‐S‐transferase; the effect being dose dependent. Carbofuran at different doses also caused sharp reduction in the activity of Na⁺‐K⁺‐ATPase. The pretreatment of vitamin E, however, showed a significant recovery in these indices. The pretreatment of rats with vitamin E offered protection from carbofuran‐induced oxidative stress.     

Study on therapeutic action of bone marrow derived mesenchymal stem cell combined with vitamin E against acute kidney injury in rats

AimsThe study aims to investigate the effect to treat acute kidney injury (AKI) with bone marrow derived mesenchymal stem cells (BMSCs) combined with vitamin E and to develop a new treatment mode for AKI preclinical study.Main methodsBMSCs were separated from rat bone marrow. Gentamicin was used as a damage factor in the culture of renal tubular epithelial cells (RTECs) in vitro. After co-cultured with BMSCs and vitamin E, cell proliferation of each group was detected with CCK-8. In vivo, BMSCs (3.3 × 10⁶ cells/kg) combined with vitamin E (80 mg/kg) were administered in AKI rats induced by gentamicin intravenously. The pathological changes, biochemical parameters and apoptosis genes after treatment were investigated furthermore.Key findingsIn co-cultured system, proliferating ability of RTECs was improved by BMSCs or vitamin E, especially for the combined group (P < 0.05). The treated rats in combined group presented the lowest serum creatinine and the highest urea nitrogen compared to non-treated rats. The improvement in renal pathological changes was followed by less necrosis, degeneration and expansion of renal tubule. Under transmission electron microscope, unclear cell structure and reduction of endoplasmic reticulum in the cytoplasm of RTECs were ameliorated with the treatment. Most apoptosis genes were up-regulated in model group while down-regulated with the therapy. Further analysis showed that the two treatments may act independently with each other.SignificanceOur data demonstrated that both BMSC and vitamin E hold therapeutic action to AKI induced by gentamicin. Especially, the combined treatment is better than BMSC or vitamin E alone.     

Ferulic acid in the treatment of post‐diabetes testicular damage: relevance to the down regulation of apoptosis correlates with antioxidant status via modulation of TGF‐β1, IL‐1β and Akt signalling

The aim of this study was to investigate the protective effect of ferulic acid at different doses (50 mg kg^?1 alternative day and 50 mg kg^?1 daily) on the streptozotocin (STZ)‐induced post‐diabetes rat testicular damage. Diabetes was induced by a single intraperitoneal injection of STZ (50 mg/kg). Rats treated with ferulic acid were given once a day orally for 10 weeks, starting 3 days after STZ injection. Testis tissue and blood samples were collected for investigating biochemical analysis, antioxidant status, sperm parameters, and histopathological, immunohistochemical and apoptotic studies. Treatment with ferulic acid to diabetic rats significantly improved the body weight, testis weight, serum insulin level, serum testosterone level and sperm parameters (viability, motility and count). Histopathological study also revealed that ferulic acid‐treated diabetic rats showed an improved histological appearance. Our data indicated that significant reduction in the activity of apoptosis by using terminal deoxyuridine triphosphate nick end‐labelling and reduced expression of transforming growth factor‐β1 and interleukin‐1β in the testis tissue of ferulic acid‐treated diabetic rats. Conversely, it was also revealed that ferulic acid‐treated diabetic rats markedly enhanced the serine/threonine protein kinase protein expression in the testis tissue. Our result suggests that ferulic acid inhibits testicular damage in diabetic rats by declining oxidative stress. Copyright © 2013 John Wiley & Sons, Ltd.     

Galangin,a natural flavonoid reduces mitochondrial oxidative damage in streptozotocin-induced diabetic rats

Objective: We designed this study to observe the effect of galangin on damaged mitochondria in the liver of diabetic rats.

Methods: Male albino Wistar rats were made diabetic by injecting streptozotocin (STZ) intraperitoneally (40?mg?kg^?1 body weight (BW)). Galangin (8?mg?kg^?1 BW) or glibenclamide (600?µg?kg^?1 BW) was given orally daily once for 45 days to both healthy and diabetic rats.

Results: Diabetic rats showed significant (P?P?P?P?P?Conclusion: From the results, we conclude that galangin could maintain liver mitochondrial function in diabetic rats.     

Effects of administration of Embelin and Curcumin on lipid peroxidation, hepatic glutathione antioxidant defense and hematopoietic system during N-nitrosodiethylamine/Phenobarbital-induced hepatocarcinogenesis in Wistar rats

The effects of administration of Embelin (EMB) and Curcumin (CUR) on lipid peroxidation, hepatic glutathione antioxidant defense and hematopoietic cells were examined during N-nitrosodiethylamine (DENA-200 mg kg⁻¹body wt, single I.P injection) initiated and Phenobarbital (PB-0.05% in drinking water orally for 13 weeks) promoted hepatocarcinogenesis in Wistar strain male albino rats. DENA/PB-induced hepatic damage was manifested by a significant drop in the hepatic glutathione antioxidant defense, increased lipid peroxidation and histological alterations like dysplasia, and atypical cells with abnormal chromatin pattern. Treatment with Curcumin (100 mg kg⁻¹body wt) and Embelin (50 mg kg⁻¹body wt) prevented the drop in hepatic glutathione antioxidant defense, decreased lipid peroxidation, minimized the histological alterations induced by DENA/PB, but showed toxic effects on the hematopoietic cells. Results indicate the beneficial effects of Embelin and Curcumin against oxidative tissue damage during chemically-induced hepatocarinogenesis in rats.     

Benzene induces haematotoxicity by promoting deacetylation and autophagy

Chronic exposure to benzene is known to be associated with haematotoxicity and the development of aplastic anaemia and leukaemia. However, the mechanism underlying benzene‐induced haematotoxicity, especially at low concentrations of chronic benzene exposure has not been well‐elucidated. Here, we found that increased autophagy and decreased acetylation occurred in bone marrow mononuclear cells (BMMNCs) isolated from patients with chronic benzene exposure. We further showed in vitro that benzene metabolite, hydroquinone (HQ) could directly induce autophagy without apoptosis in BMMNCs and CD34⁺ cells. This was mediated by reduction in acetylation of autophagy components through inhibiting the activity of acetyltransferase, p300. Furthermore, elevation of p300 expression by Momordica Antiviral Protein 30 Kd (MAP30) or chloroquine reduced HQ‐induced autophagy. We further demonstrated that in vivo, MAP30 and chloroquine reversed benzene‐induced autophagy and haematotoxicity in a mouse model. Taken together, these findings highlight increased autophagy as a novel mechanism for benzene‐induced haematotoxicity and provide potential strategies to reverse this process for therapeutic benefits.     

Effect of feeding supplemental copper on performance,fatty acid profile and on cholesterol contents and oxidative stability of meat of rabbits

One hundred and four rabbits, five weeks old at the beginning of the experiment, were divided into four groups according to a feed additive treatment. Rabbits of the 1st, 2nd, 3rd and 4th group were fed a basal granulated feed (control), basal feed supplemented with CuSO₄ · 5H₂O at 50mg Cu · kg^‐1, basal feed supplemented with 150mg Cu · kg^‐1, and the latter feed supplemented with 100mg · kg^‐1 vitamin E, respectively. The duration of the experiment was 42 days. Addition of Cu at 150mg · kg.^‐1 increased weight gain non‐significantly by 9.1%. This effect was the most pronounced in the first two weeks of fattening. The lowest mortality was observed in rabbits fed the highest amount of additives (7.7% vs. 19.2% in the control). Rabbits were slaughtered at the age of 11 weeks. Neither treatment influenced proportions of saturated, monounsaturated and polyunsaturated fatty acids in lipids extracted from the loin and hindleg muscles. In rabbits fed the highest amount of copper and vitamin E, the cholesterol concentration was significantly decreased by 13.6% and 17.9% in the loin and hindleg meat, respectively. Effects of Cu added at 50mg · kg^‐1 were marginal. Copper had no effect on the oxidative stability of meat, measured as thiobarbituric acid‐reactive substances in meat stored at 4°C for 0, 3 and 8 days. Vitamin E added in excess of nutritional requirement improved the oxidative stability of meat. In copper‐fed rabbits, Cu accumulated in the liver, but not in muscles. Feeding of the basal feed for 7 days to rabbits previously fed copper sulphate decreased the hepatic Cu concentration by 14.0 to 24.4%     

Regulation of expression of antioxidant enzymes by vitamin E and curcumin in <Emphasis Type="SmallCaps">l</Emphasis>-thyroxine-induced oxidative stress in rat renal cortex

The present study investigates the antioxidative effects of vitamin E and curcumin against l-thyroxine (T₄)-induced oxidative stress in renal cortex of adult male rats. Rats were made hyperthyroid by administration of l-thyroxine (0.0012%) in their drinking water for 30 days. Vitamin E (200 mg/kg body weight/day) and curcumin (30 mg/kg body weight/day) were supplemented singly or in combination orally for 30 days along with l-thyroxine treatment. The elevated level of oxidative stress parameters (lipid peroxidation and protein carbonylation) and decline level of small antioxidant molecules (reduced glutathione and ascorbic acid) in renal cortex of T₄-treated rats were restored back by supplementation of vitamin E or/and curcumin. Increased superoxide dismutase and catalase activities in kidney cortex of T₄-treated rats were ameliorated in response to vitamin E or/and curcumin treatment. The elevated translated product of Cu/Zn-SOD, Mn-SOD and catalase in T₄-treated rats were differentially reduced by the administration of vitamin E and curcumin independently or in combination. Cu/Zn-SOD expression was ameliorated by both vitamin E and curcumin independently or in combination, whereas Mn-SOD expression was ameliorated by the supplementation of vitamin E or curcumin independently. However, the expression of catalase was alleviated by only supplementation of vitamin E to T₄-treated rats. The results suggest that both vitamin E and curcumin may play an important role in protecting T₄-induced oxidative stress in rat renal cortex by differentially modulating the activities of antioxidant enzymes and oxidative stress parameters.