Superoxide Dismutase Glutathione Peroxidase Research Articles

Effects of selenium nanoparticles on larval development, ontogeny of antioxidant enzymes and fatty acid profile in Arabian yellowfin seabream (Acanthopagrus arabicus)

Selenium (Se) is an essential trace element that has vital effects on growth, antioxidant capacity and early development in marine fish larvae. However, traditional livefoods such as rotifer and artemia lack of Se. In this regard, a 50-day feeding experiment was conducted in order to examine the effects of Rotifer and Artemia enrichment with selenium nanoparticles (SeNPs) on growth, antioxidant capacity and fatty acid profile of Arabian yellowfin seabream (Acanthopagrus arabicus) larvae. Four levels of SeNPs were used to prepare the experimental emulsions,including control (0), 0.5, 1.0 and 5 mg SeNPs L−1. Larvae were stocked at density of 50 larvae L−1 into twelve 250-L cylindrical tanks. Tanks supplied with seawater (23 ± 1 ºC; 40.0 ± 1.0 g L−1). Green water was used from day first until 20 days after hatch (DAH). Rotifers (15 ml−1) were offered to larvae from day 2–21 DAH and Artemia metanauplii (1–3 Artemia ml−1) were offered to larvae from day 18–45 DAH. Fish were sampled at 0, 7, 10, 15, 22, 30, 40, 45, 50 DAH. The Se concentration in the livefoods and larval whole body linearly increased with the increment of SeNPs level in the experimental emulsions. Larvae wet weight showed quadratic response and increased with SeNPs up to 1 mg mg SeNPs/L, then decreased in SeNPs (5.0) group. The activity of antioxidant enzymes including catalase, superoxide dismutase glutathione peroxidase, and total antioxidant capacity increased but malondialdehyde level decreased in larvae fed the SeNPs-enriched livefoods and showed both linear and quadratic responses. Lysozyme activity in the whole body of larvae fed SeNPs-enriched livefoods had both linear and quadratic responses and in the most of the sampling times was higher than the control group. Docosahexaenoic acid (DHA) level in the livefoods and larval whole body increased with SeNPs. In conclusion, livefoods enrichment with SeNPs at 1 mg L−1 is recommended to elevate the antioxidant capacity and non-specific immune response in A. arabicus larvae.

Selenium Abrogates Tenofovir/Lamivudine/Efavirenz-Induced Hepatotoxicity in Rats

Background: The therapeutic benefit of tenofovir/lamivudine/efavirenz (TLE) in the treatment of human immunodeficiency virus can be truncated by the occurrence of hepatotoxicity. This study evaluated the protective effect of selenium (Se) against hepatotoxicity induced by TLE in albino rats. Materials and Methods: Adult male albino rats (n = 40) randomized into four groups (n = 10) were used. Group 1 (Control) orally received normal saline (0.2 mL) daily. Group 2 orally received Se (0.1 mg/kg) daily. Group 3 orally received TLE (8.6/8.6/17.1 mg/kg) daily. Group 4 orally received Se (0.1 mg/kg) and TLE (8.6/8.6/17.1 mg/kg) daily. All rats were treated for 90 days. After treatment, the rats were euthanized, and serum samples were centrifuged from blood samples and assessed for liver function markers. Liver samples were harvested and evaluated for morphological changes and biochemical parameters. Results: Impaired liver redox status in TLE-treated rats was characterized by remarkable (P < 0.001) decreases in glutathione peroxidase superoxide dismutase, catalase, and glutathione levels with remarkable (P < 0.001) increases in malondialdehyde levels when compared to control. The alterations in liver function markers were marked by remarkable (P < 0.001) increases in serum aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, alkaline phosphatase, gamma-glutamyl transferase, conjugated bilirubin and total bilirubin levels when compared to control. Hepatocyte necrosis and fatty change were observed in TLE-treated rats. However, TLE-induced hepatotoxic changes were significantly (P < 0.01) reversed in Se supplemented rats when compared to TLE. Conclusion: Se may be clinically effective against hepatotoxicity caused by TLE.

Moderation of doxorubicin-induced nephrotoxicity in Wistar rats by aqueous leaf-extracts of Chromolaena odorata and Tridax procumbens.

Background:The major draw-back of doxorubicin's use in chemotherapy is its toxicity on various organs including the kidneys. This study investigated the potential protective role of aqueous leaf-extracts of Chromolaena odorata and Tridax procumbens against nephrotoxicity induced by doxorubicin.Methods:To this end, their impact on plasma biomarkers of kidney function, as well as renal lipid profile, biomarkers of oxidative stress, electrolyte profile and activities of renal ATPases was monitored in doxorubicin treated rats. Metformin (250 mg/kg body weight, orally) and the extracts (50, 75 and 100 mg/kg, orally) were daily administered for 14 days; while nephrotoxicity was induced with doxorubicin (15 mg/kg, intra-peritioneally), once on the 12th day of study.Results:The plasma concentrations of creatinine, and urea; as well as the renal malondialdehyde, cholesterol, calcium and sodium concentrations in the Test control, were significantly (P < .05) higher than those of all the other groups. However, the renal concentrations of ascorbic acid, chloride, magnesium and potassium, and the renal activities of catalase, glutathione peroxidase superoxide dismutase, Ca2+-ATPase, Mg2+-ATPase and Na+,K+-ATPase in the Test control were significantly (P < .05) lower than those of all the other groups.Conclusions:Pre-treatment with the extracts and metformin boosted endogenous antioxidants, and prevented doxorubicin-induced renal damage, as indicated by the attenuation of doxorubicin-induced renal oxidative stress, as well as the attenuation of doxorubicin-induced adverse alterations in renal cholesterol, ATPases and electrolyte balance, and plasma biomarkers of kidney function, and keeping them at near-normal values.

The Comparison of Parameters of Oxidative Stress in Native Rat Livers Between Different Immunosuppressive Regimens.

BackgroundIt is thought that immunosuppressive treatment, besides anti-rejection properties, leads to pathological changes within the organ due to activation of mechanisms associated with oxidative stress. The aim of this study was to examine the parameters of oxidative stress in the livers of rats treated with the most commonly used transplant recipient drug regimens.Material/MethodsThe rat livers were obtained from archival material obtained from the previously performed experiment. Malondialdehyde (MDA), reduced glutathione (GSH) concentrations, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities were analyzed.ResultsOnly the group treated with tacrolimus (T), mycophenolate mofetil (M), and prednisone (P), the TMP group, showed a slight increase in lipid peroxide concentration compared to the control group, though the difference was not statistically significant. Comparison of lipid peroxide concentration between the other treatment combinations and the control group showed a significant decrease. Additionally, a difference in lipid peroxide concentrations in the livers was observed between the cyclosporine A (C) group and tacrolimus (T) group. Alterations of other oxidative stress parameters were also observed in different regimens.ConclusionsLong-lasting immunosuppressive treatment does indeed affect redox status; however, the antioxidant defenses of the liver against the effects of excess hydrogen peroxide are efficient, so the superoxide dismutase/glutathione peroxidase (SOD/GPx) and superoxide dismutase/catalase (SOD/CAT) ratios were not significant.

Carvacrol protects against spinal cord injury in rats via suppressing oxidative stress and the endothelial nitric oxide synthase pathway.

Carvacrol (CAR) is a naturally occurring phenolic monoterpene and has been demonstrated to possess a spectrum of pharmacological actions. The present study was designed to assess the neuroprotection of CAR against spinal cord injury (SCI) in rats and to identify the underlying mechanisms. SCI was induced using the modified weight‑drop method in Wistar rats. CAR or saline was administered at doses of 25, 50 and 100 mg/kg for 46 days. Neuronal function following SCI was evaluated using the Basso, Beattie and Bresnahan (BBB) locomotor rating scale. Spinal cord edema was assessed by measuring the water content in spinal cord tissues. The oxidative indicators, including malondialdehyde, catalase, superoxide dismutase glutathione peroxidase and 8‑isoprotane as well as endothelial nitric oxide synthase (eNOS) activity and caspase‑3 were measured using corresponding commercial kits. The protein expression of eNOS and B cell lymphoma‑2 (Bcl‑2) as well as Bcl‑2‑associated X protein (Bax) was analyzed by western blot analysis. The SCI‑induced rats demonstrated marked reductions in BBB scores. CAR treatment recovered neurological function with decreasing BBB scores. CAR was found to have inhibitory effects on the water content in the spinal cord, oxidative stress, eNOS, nitric oxide production and apoptosis‑associated molecules, including Bax and caspase‑3 as well as promoting Bcl-2 expression in SCI-induced rats. These results suggested that CAR protects against SCI via mediating oxidative stress and the eNOS signaling pathway.

A new approach using biomarkers to elucidate the regression state of the invasive alga Caulerpa taxifolia in waters around the Balearic Islands (Western Mediterranean Sea)

Invasive algae alter the structure and function of ecosystems. The green alga Caulerpa taxifolia is an invasive alga introduced in the Mediterranean Sea, whereas Caulerpa prolifera is a native species in Mediterranean waters. The aim of the current work was to determine the oxidative status of both Caulerpa species by means of biomarker measures as a possible indicator of the regression state of C. taxifolia in waters around the Balearic Islands (western Mediterranean Sea). The levels of markers of lipid peroxidation, glutathione concentration, activities of antioxidant enzymes and caulerpenyne production were measured in C. prolifera and C. taxifolia fronds. The concentration of the end product of lipid peroxidation, malondialdehyde, was significantly higher in C. taxifolia than in C. prolifera samples. Antioxidant enzyme activities, namely superoxide dismutase glutathione peroxidase and glutathione reductase, as well as the reduced glutathione : glutathione disulfide ratio were lower in C. taxifolia than in C. prolifera, although the concentrations of malondialdehyde were higher in the alien species. No differences were found in catalase activity or in the concentration of caulerpenyne. In conclusion, the invasive alga C. taxifolia presented a more oxidised status, which could be related to its regression in Mallorcan coastal waters.

Protective effect of pravastatin against mercury induced vascular cells damage: Erythrocytes as surrogate markers

In the present study we investigated the protective effect of pravastatin (PRV) against mercury-induced cellular damage. Human erythrocytes were incubated with PRV, HgCl2 and HgCl2 pretreated with PRV. Our results revealed that incubation of erythrocytes with HgCl2 induces a significant increase the ratios of superoxide dismutase/glutathione peroxidase (SOD/GPx), superoxide dismutase/catalase (SOD/CAT), oxidized/reduced glutathione (GSSG/GSH), malondialdehyde(MDA) and protein carbonyl(PCO) by 60%, 50%, 333%, 400% and 208% respectively. Whereas, prior incubation of erythrocytes with PRV maintains these parameters at values similar to control cells. Furthermore, the level of nitrite in erythrocytes decreases significantly on treatment with HgCl2, whereas it remains similar to the control when pretreated with PRV. Also, there was an increase in erythrocytes hemolysis when treated with HgCl2, whereas it remained the like to the control when pretreated with PRV. In conclusion, PRV pretreatment maintained the erythrocytes oxidant/antioxidant balance and nitrite level during mercury exposure. Consequently, PRV pretreatment is worthy of further investigation in the reduction of the cardiovascular risk of mercury.

Antioxidant role of propolis extract against oxidative damage of testicular tissue induced by insecticide chlorpyrifos in rats

Pesticides induce oxidative stress leading to generate free radicals and alternate the antioxidant or oxygen free radical scavenging enzyme system. This study was conducted to investigate the oral toxicity of chlorpyrifos toward male rat and the oxidative stress of the sub-lethal dose (9mg/kg; 1/25 LD50) on the lipid peroxidation level (LPO), reduced glutathione content (GSH) and antioxidant enzymes; catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities of testicular tissue. Also, the protective effects of propolis extract (50mg/kgb.w.) alone or in combination with chlorpyrifos were investigated. The oral administration of chlorpyrifos significantly caused elevation in LPO level by 1.79-fold as compared to control. The activities of antioxidant enzymes including CAT, SOD, GPx and GST were decreased significantly (23.66%, 27.75%, 29.13% and 11.52%) as well as the level of GSH decreased by 21.97% in testicular tissue as compared to control animals. Co-administration of propolis extract with chlorpyrifos or alone in male rats decreased LPO level, normalized CAT, SOD GPx and GST activities, while GSH content was increased in testicular tissue. We conclude that propolis extract significantly reduces chlorpyrifos-induced oxidative stress in rat testis and the protective effect of the pre-treatment with propolis extract as attenuating agent could be due to its antioxidant properties.

Enhancement of immunity and disease resistance in the white shrimp, Litopenaeus vannamei, by the probiotic, Bacillus subtilis E20

Effects of Bacillus subtilis E20 isolated from fermented soybean on immune parameters and the disease resistance of the white shrimp ( Litopenaeus vannamei) after 98 days of B. subtilis E20 feeding were evaluated in this study. Shrimp fed B. subtilis E20-containing diets at concentrations of 10 6 (E206), 10 7 (E207), and 10 8 (E208) cfu kg −1, respectively, had significantly increased survival rates of 13.3%, 16.7%, and 20%, compared to the control (fed no probiotic) after being challenged with Vibrio alginolyticus. There were no significant differences in the total hemocyte count, respiratory burst, or superoxide dismutase glutathione peroxidase among all treatments. Shrimp fed a higher concentration of the probiotic (E208) exhibited significant increases in phenoloxidase activity, phagocytic activity, and clearance efficiency compared to control shrimp. In addition, B. subtilis E20 showed a weaker inhibitory effect against the growth of Aeromona hydrophila with around a 0.3-cm inhibitory zone, but showed no inhibitory effects against other selected pathogens, such as white shrimp pathogens: V. alginolyticus and Vibrio vulnificus. These results suggest that the increased resistance of shrimp after B. subtilis E20 consumption occurs through immune modifications, such as increases in phenoloxidase activity, phagocytic activity, and clearance efficiency against V. alginolyticus.

An Investigation of the response of lymphoblastoid cells to hydrogen peroxide-derived oxidative stress

The synthesis of heat shock proteins (HSPs) may play a significant role in the mechanism of cellular protection against oxidative injury [ I , 21. We have shown that T-lymphoid (Molt-3) cells exhibit enhanced susceptibility to H202-induced cytogenetic damage and that these cells also have low levels of intracellular catalase activity [3]. The aim of this study was to investigate the response of human T-lymphoid cells (Molt-3) to H202-derived oxidative stress. The endpoints we analysed were HSP synthesis and cellular antioxidant enzyme activities. Molt-3 cells were maintained in RPMI 1640 containing 10 % (v/v) FCS, 100 IU/ml streptomycin/penicillin and incubated at 37'C in 9 5 5 % air:CO2 humidified athmosphere. Previous experiments had shown that a dose of 10 pM H202 was non-toxic to Molt-3 cells and a dose of 100 pM H202 was cytotoxic. In the light of these findings, the following treatment groups were set up; control cells where no H202 was added; cells pretreated with a single dose of 10 pM H202, incubated for 18 h at 37 'C and then challenged with a 30 min exposure to 100 pM H202. cells were washed free of H202 and were then further incubated for 72h. Other treatment groups consisted of cells receiving pretreatment with 10 pM H202 only or receiving 100 pM H202 challenge only. Cell viability was determined by the Trypan-Blue exclusion test. Control and H202 treated cells were harvested at 72 h post challenge treatment and total cell lysates prepared by sonication. Cellular antioxidant assays were then performed for superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT), according to the methods described 14-61 respectively. To assess HSP synthesis treated cells were cultured in RPMI 1640 supplemented with 20 pCi/ml L-[35S]-methionine (specific activity > lo00 Ci/mmol), harvested and washed twice in PBS. After sonication total cell lysates were solubilized in 2% (w/v) SDS. 10% (v/v) glycerol, 62 mM Tris-HCI. pH 6.8. 5% (v/v) mercaptoethanol. 0.0025% (wh.) bromophenol blue. Samples were boiled and subjected to I-D SDS-PAGE. HSPs were identified by probing PVDF membranes with anti-Hsc/Hsp 70 (C92F3A-5) recognising both constitutive and inducible forms, anti Hsp-70 (C92F3A-5) inducible form only and anti-heme-oxygenase (HO1) (1:lOOO dilution, v/v), and detection was achieved with a reporter alkaline phosphatase (AP)-linked reporter antibody (1:3O,o00 dilution, v/v) and a AP staining kit. Table 1 compares the cellular antioxidant enzyme status of Molt-3 cells pretreated with 10 pM H202 with control groups. Following pretreatment there was a marked increase intracellular GPx activity i.e., 62 f 10.00 mU/mg protein (P< 0.05) compared to 38 f 8.8 mU mg protein for untreated cells. There was no significant alteration in the activities of SOD and CAT in pretreated and challenged groups. These results show that GPx activity increases in Molt-3 cells in response to a non-toxic H202 exposure. Table 1. lntracellular antioxidant enzyme activities in Molt-3 cells in culture following exposure to H202. Treatment SOD GPx . CAT Group (U/mg) (mU/mg) (Uhng)