Chlorpyrifos Induced Region Specific Vulnerability in Rat CNS and Modulation by Age and Cold Stress: An Interactive Study

Chlorpyrifos (CPF), an organophosphorus insecticide is known to cause ill health in non-target animals by inducing oxidative stress. In this study influence of cold stress (15°C and 20°C) and age as modulating factors on CPF induced oxidative stress was addressed to assess age-related differences and vulnerability in central nervous system of rats. The results indicated an interaction with age and cold exposure resulting in marked decreased activity levels of SOD (P < 0.05), CAT (P < 0.05), GPx (P < 0.05), GST (P < 0.05) followed by increased MDA (P < 0.05) and decreased GSH levels (P < 0.05). The ANOVA and Post-hoc analysis showed that antioxidant enzymes decreased significantly (P < 0.05) on CPF exposure. Moreover synergistic action of CPF and cold stress at 15°C caused higher inhibition on comparison with CPF and cold stress alone and together at 20°C indicating the extent of peroxidative damage in discrete regions of CNS. Further this study showed young individuals to be more sensitive than adults.     

模拟失重不同时长对大鼠抑郁样行为的影响

目的 本研究旨在观察不同持续时间的模拟失重对大鼠抑郁样行为和海马超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的影响，以探究其影响及可能的作用机制。方法 采用后肢悬挂（HLS）尾吊法模拟大鼠失重状态。将大鼠分为对照组和不同模拟失重时间尾吊组（尾吊时长分别为1、2、3、4周）。采用旷场实验（OFT）、新物体识别实验（NORT）、强迫游泳实验（FST）观察大鼠抑郁样行为，采用酶联免疫吸附试验（ELISA）法测定海马SOD和CAT活性。结果 OFT结果显示，与对照组相比，HLS不同时间大鼠的僵滞时间增加（P<0.05，P<0.01）。在NORT中，与对照组相比，HLS不同时间大鼠对新物体的探索潜伏期增加，探索次数和时间减少（P<0.05，P<0.01）。在FST中，与对照组相比，HLS不同时间大鼠在FST中的不动时间增加，攀爬次数减少（P<0.05，P<0.01）。与对照组相比，HLS不同时间组大鼠海马组织中SOD和CAT水平均下降（P<0.05，P<0.01）。结论 短时间或长时间的失重都会导致大鼠产生类抑郁样行为。     

The hepatoprotective effects of Hypericum perforatum L. on hepatic ischemia/reperfusion injury in rats

Little is known about the effective role of Hypericum perforatum on hepatic ischemia–reperfusion (I/R) injury in rats. Hence, albino rats were subjected to 45 min of hepatic ischemia followed by 60 min of reperfusion period. Hypericum perforatum extract (HPE) at the dose of 50 mg/kg body weight (HPE₅₀) was intraperitonally injected as a single dose, 15 min prior to ischemia. Rats were sacrificed at the end of reperfusion period and then, biochemical investigations were made in serum and liver tissue. Liver tissue homogenates were used for the measurement of malondialdehyde (MDA), catalase (CAT) and glutathione peroxidase (GPx) levels. At the same time alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were assayed in serum samples and compared statistically. While the ALT, AST, LDH activities and MDA levels were significantly increased, CAT and GPx activities significantly decreased in only I/R-induced control rats compared to normal control rats (p < 0.05). Treatment with HPE₅₀ significantly decreased the ALT, AST, LDH activities and MDA levels, and markedly increased activities of CAT and GPx in tissue homogenates compared to I/R-induced rats without treatment–control group (p < 0.05). In oxidative stress generated by hepatic ischemia–reperfusion, H. perforatum L. as an antioxidant agent contributes an alteration in the delicate balance between the scavenging capacity of antioxidant defence systems and free radicals in favour of the antioxidant defence systems in the body.     

Trypanosoma evansi: Adenosine deaminase activity in the brain of infected rats

The study was undertaken to evaluate changes in the activity of adenosine deaminase (ADA) in brains of rats infected by Trypanosoma evansi. Each rat was intraperitoneally infected with 10⁶ trypomastigotes either suspended in fresh (group A; n = 13) and cryopreserved blood (group B; n = 13). Thirteen animals were used as control (group C). ADA activity was estimated in the cerebellum, cerebral cortex, striatum and hippocampus. No differences (P > 0.05) in ADA activity were observed in the cerebellum between infected and non-infected animals. Significant (P < 0.05) reductions in ADA activity occurred in cerebral cortex in acutely (day 4 post-infection; PI) and chronically (day 20 PI) infected rats. ADA activity was significantly (P < 0.05) decreased in the hippocampus in acutely infected rats, but significantly (P < 0.05) increased in the chronically infected rats. Significant (P < 0.05) reductions in ADA activity occurred in the striatum of chronically infected rats. Parasites could be found in peripheral blood and brain tissue through microscopic examination and PCR assay, respectively, in acutely and chronically infected rats. The reduction of ADA activity in the brain was associated with high levels of parasitemia and anemia in acute infections. Alterations in ADA activity of the brain in T. evansi-infected rats may have implications for pathogenesis of the disease.     

Amelioration of altered antioxidant status and membrane linked functions by vanadium andTrigonella in alloxan diabetic rat brains

Trigonella foenum graecum seed powder (TSP) and sodium orthovanadate (SOV) have been reported to have antidiabetic effects. However, SOV exerts hypoglycemic effects at relatively high doses with several toxic effects. We used low doses of vanadate in combination with TSP and evaluated their antidiabetic effects on antioxidant enzymes and membrane-linked functions in diabetic rat brains. In rats, diabetes was induced by alloxan monohydrate (15 mg/100 g body wt.) and they were treated with 2 IU insulin, 0.6 mg/ml SOV, 5% TSP and a combination of 0.2 mg/ml SOV with 5% TSP for 21 days. Blood glucose levels, activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), Na⁺/K⁺ ATPase, membrane lipid peroxidation and fluidity were determined in different fractions of whole brain after 21 days of treatment. Diabetic rats showed high blood glucose (P < 0.001), decreased activities of SOD, catalase and Na⁺/K⁺ ATPase (P < 0.01,P < 0.001 andP < 0.01), increased levels of GPx and MDA (P < 0.01 andP < 0.001) and decreased membrane fluidity (P < 0.01). Treatment with different antidiabetic compounds restored the above-altered parameters. Combined dose ofTrigonella and vanadate was found to be the most effective treatment in normalizing these alterations. Lower doses of vanadate could be used in combination with TSP to effectively counter diabetic alterations without any toxic effects.     

Betaine Elevates Ovarian Antioxidant Enzyme Activities and Demonstrates Methyl Donor Effect in Non-Pregnant Rats

Chronic alcoholism leads to infertility in male and female rats, and antioxidant enzymes form the first line against oxidative stress in organisms. In recent years, betaine has shown beneficial effects on various tissues, and this study has attempted to clarify antioxidant and methyl donor properties of betaine in the rat ovary. For this purpose, the sexually matured Sprague-Dawley female rats were divided into Control, Ethanol (EtOH), Betaine, and Betaine?+?EtOH groups. Administration of betaine in Betaine?+?EtOH group significantly increased CAT activity when compared to the other groups (P?<?0.05). GPx activity increased significantly in Betaine and Betaine?+?EtOH groups as compared to controls (P?<?0.05). Interestingly, GPx and CAT activities insignificantly increased (in order compensatory) in EtOH group to suppress oxidative stress. In contrast, SOD activity decreased insignificantly in EtOH group compared to Betaine?+?EtOH and control groups (P?>?0.05). TBARS concentration (as a lipid peroxidation marker) significantly increased in ethanol-treated rats as compared to controls, while total homocysteine concentration significantly decreased in betaine-treated rats in comparison with EtOH group. Regarding to oestrous cycles, ethanol-treated animals had irregular estral cycle and persistent oestrous phase compared to controls and betaine-treated rats. In conclusion, these results demonstrate for the first time the antioxidant and methyl donor properties of betaine in the rat ovary. Thus, betaine might be used as a potential therapy in hyperhomocysteinemia and partial infertility mediated by oxidative stress in females.     

Cyclosporine A induced changes to plasma and erythrocyte antioxidant defences

Abstract

Organ transplant recipients develop pronounced cardiovascular disease, and decreased antioxidant capacity in plasma and erythrocytes is associated with the pathogenesis of this disease. These experiments tested the hypothesis that the immunosuppressant cyclosporine A (CsA) alters erythrocyte redox balance and reduces plasma antioxidant capacity. Female Sprague-Dawley rats were randomly assigned to a control or CsA treated group. Treatment animals received 25 mg/kg/day of CsA via intraperitoneal injection for 18 days. Control rats were injected with the same volume of the vehicle. Three hours after the final CsA injection, rats were exsanguinated and plasma analysed for total antioxidant status (TAS), α-tocopherol, malondialdehyde (MDA), and creatinine. Erythrocytes were analysed for superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glucose-6-phosphate dehydrogenase (G6PD) activities, α-tocopherol, and MDA. CsA administration resulted in a significant (P < 0.05) decrease in plasma TAS and significant increases (P < 0.05) in plasma creatinine and MDA. Erythrocyte CAT was significantly (P < 0.05) increased in CsA treated rats compared to controls. There were no significant differences (P > 0.05) in erythrocyte SOD, GPX, G6PD, α-tocopherol or MDA between groups. In summary, CsA alters erythrocyte antioxidant defence and decreases plasma total antioxidant capacity.     

Preventive role of gallic acid on hepatic ischemia and reperfusion injury in rats

There is little information about the hepatoprotective effects of gallic acid against ischemia–reperfusion (I/R) damage. Animals were subjected to I/R. Gallic acid at doses of 50 and 100 mg/kg body weight (bw) were injected as a single dose prior to ischemia. Liver tissue homogenates were used for the measurement of malondialdehyde (MDA), catalase (CAT) and glutathione peroxidase (GPx) levels. At the same time alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were assayed in serum samples and compared statistically. While the ALT, AST, LDH activities and MDA levels were significantly increased, CAT and GPx activities significantly decreased in only I/R-induced control rats compared to normal control rats (P < 0.05). Treatment with gallic acid at a dose of 100 mg/kg bw significantly decreased the ALT, AST, LDH activities and MDA levels, and markedly increased activities of CAT and GPx in tissue homogenates compared to I/R-induced rats with no treatment group (P < 0.05). In oxidative stress generated by hepatic ischemia–reperfusion, gallic acid contributes partially an alteration in the delicate balance between the scavenging capacity of antioxidant defense systems and free radicals in favour of the antioxidant defense systems in the body.     

Neuroprotective effects of Caffeic acid phenethyl ester on experimental traumatic brain injury in rats

The aim of this study was to evaluate the therapeutic efficacy of caffeic acid phenethyl ester (CAPE) with an experimental traumatic brain injury (TBI) model in rats. Twenty-four adult male Sprague–Dawley rats were randomly divided into three groups of 8 rats each: control, TBI, and TBI + CAPE treatment. In TBI and TBI + CAPE treatment groups, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 4 h after the onset of injury. Brain tissues were removed for biochemical and histopathological investigation. To date, no biochemical and histopathological changes of neurodegeneration in the frontal cortex after TBI in rats by CAPE treatment have been reported. The TBI significantly increased tissue malondialdehyde (MDA) levels, and significantly decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, but not tissue catalase (CAT) activity, when compared with controls. The administration of a single dose of CAPE (10 μmol/kg) 15 min after the trauma has shown protective effect via decreasing significantly the elevated MDA levels and also significantly increasing the reduced antioxidant enzyme (SOD and GPx) activities, except CAT activity. In the TBI group, severe degenerative changes, shrunken cytoplasma and extensively dark picnotic nuclei in neurons, as well as vacuolization indicating tissue edema formation. The morphology of neurons in the CAPE treatment group was well protected. The number of neurons in the trauma alone group was significantly less than that of both the control and TBI +CAPE treatment groups. The caspase 3 immunopositivity was increased in degenerating neurons of the traumatic brain tissue. Treatment of CAPE markedly reduced the immunoreactivity of degenerating neurons. TBI caused severe degenerative changes, shrunken cytoplasma, severely dilated cisternae of endoplasmic reticulum, markedly swollen mitochondria with degenerated cristae and nuclear membrane breakdown with chromatin disorganization in neurons of the frontal cortex. In conclusion, the CAPE treatment might be beneficial in preventing trauma-induced oxidative brain tissue damage, thus showing potential for clinical implications. We believe that further preclinical research into the utility of CAPE may indicate its usefulness as a potential treatment on neurodegeneration after TBI in rats.     

Evaluation of oxidative DNA damage and antioxidant defense in patients with nasal polyps

Abstract

Objectives

The presence of inflammatory cells indicates the development of epithelial cell injury in nasal polyposis (NP) and the potential for production of high levels of reactive oxygen and nitrogen species. The aim of our study was to clarify the role of oxidative stress and antioxidant status in the deterioration accompanying NP.

Methods

Twenty patients (11 men) aged 47.2 ± 17.0 years with nasal polyps were included in the study. Twenty healthy subjects (7 men) aged 48.2 ± 15.3 years formed the control group. The erythrocyte activities of antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), and plasma nitric oxide (NO) concentrations were measured. An alkaline comet assay was used to determine the extent of blood lymphocyte DNA damage of oxidized purines as glicosylo-formamidoglicosylase (Fpg) sites, and oxidized pyrimidines as endonuclease III (Nth) sites.

Results

A significant increase of NO (P < 0.05) and non-significant decreases of SOD (P > 0.05), CAT (P > 0.05), and GPx (P > 0.05) were seen in NP patients compared to healthy controls. The level of blood lymphocyte oxidative DNA damage in NP patients was significantly higher compared to the control group (P = 0.01).

Discussion

The blood lymphocyte DNA damage level increased in patients with NP. Elevated DNA damage may be related to overproduction of reactive oxygen and nitrogen species and/or decreased antioxidant protection.     

The Effect of n-acetylcysteine and Deferoxamine on Exercise-induced Oxidative Damage in Striatum and Hippocampus of Mice

The aim of this study was to analyze the effects of intense exercise on brain redox status, associated with antioxidant supplementation of N-acetylcysteine (NAC), deferoxamine (DFX) or a combination of both. Seventy-two C57BL-6 adult male mice were randomly assigned to 8 groups: control, NAC, DFX, NAC plus DFX, exercise, exercise with NAC, exercise with DFX, and exercise with NAC plus DFX. They were given antioxidant supplementation, exercise training on a treadmill for 12 weeks, and sacrificed 48 h after the last exercise session. Training significantly increased (P < 0.05) soleus citrate synthase (CS) activity when compared to control. Blood lactate levels classified the exercise as intense. Exercise significantly increased (P < 0.05) oxidation of biomolecules and superoxide dismutase activity in striatum and hippocampus. Training significantly increased (P < 0.05) catalase activity in striatum. NAC and DFX supplementation significantly protected (P < 0.05) against oxidative damage. These results indicate intense exercise as oxidant and NAC and DFX as antioxidant to the hippocampus and the striatum.     

Aminoguanidine and N-acetyl-cysteine supress oxidative and nitrosative stress in EAE rat brains

Abstract

Experimental autoimmune encephalomyelitis (EAE) is a well-established animal model of human multiple sclerosis (MS). We have evaluated the role of oxidative and nitrosative stress, as the causal factors in the development of EAE, responsible for the damage of cardinal cellular components, such as lipids, proteins and nucleic acids, resulting in demyelination, axonal damage, and neuronal death. EAE was induced in female Sprague-Dawley rats, 3 months old (300 ± 20 g), by immunization with myelin basic protein in combination with Complete Freund's adjuvant (CFA). The animals were divided into seven groups: control, EAE, CFA, EAE + aminoguanidine (AG), AG, EAE + N-acetyl-l-cysteine (NAC) and NAC. The animals were sacrificed 15 days after EAE induction, and the levels of nitrosative and oxidative stress were determined in 10% homogenate of the whole encephalitic mass. In EAE rats, brain NO production and MDA level were significantly increased (P < 0.001) compared to the control values, whereas AG and NAC treatment decreased both parameters in EAE rats compared to EAE group (P < 0.001). Glutathione (GSH) was reduced (P < 0.001) in EAE rats in comparison with the control and CFA groups, but increased in EAE + AG and EAE + NAC group compared to the EAE group (P < 0.01). Superoxide dismutase (SOD) activity was significantly decreased (P < 0.001) in the EAE group compared to all other experimental groups. The clinical expression of EAE was significantly decreased (P < 0.05) in the EAE groups treated with AG and NAC compared to EAE rats, during disease development.

The obtained results prove an important role of oxidative and nitrosative stress in the pathogenesis of EAE, whereas AG and NAC protective effects offer new possibilities for a modified combined approach in MS therapy.     

Acetyl-<Emphasis Type="SmallCaps">l</Emphasis>-carnitine prevents carbon tetrachloride-induced oxidative stress in various tissues of Wistar rats

Acetyl-l-carnitine (ALCAR) has been shown to prevent experimental selenite cataractogenesis, a manifestation of oxidative stress, but little is known about its potential in other settings of oxidative stress. The present study was based on the hypothesis that ALCAR prevents carbon tetrachloride (CCl₄)-induced oxidative stress in vital tissues. Male albino Wistar rats were divided into three groups, each of six rats. Group I (control) rats received only vehicle (1 ml/kg b.w.) for 4 days; Group II (CCl₄-exposed, untreated) rats received CCl₄ (2 ml/kg b.w.) on the second and third days and vehicle on the first and fourth days; Group III (CCl₄-exposed, ALCAR-treated) rats received ALCAR (200 mg/kg b.w.) for 4 days and CCl₄ on the second and third days. All administrations were made intraperitoneally. After the experimental period, significantly (P < 0.05) elevated mean serum levels of aspartate transaminase, alanine transaminase, alkaline phosphatase, and lactate dehydrogenase were observed in Group II rats when compared to Group I and Group III rats. The mean levels of vitamin C, vitamin E, and reduced glutathione and the mean activities of superoxide dismutase, catalase, and glutathione peroxidase were significantly (P < 0.05) lower in samples of hemolysate and of liver, kidney, and brain tissues of Group II rats than those in Group I and Group III rats. The mean level of lipid peroxidation was significantly (P < 0.05) higher in Group II rats than that in Group I and Group III rats. Moreover, the CCl₄-induced upregulation of inducible nitric oxide synthase expression was prevented by ALCAR in the liver and brain tissues. These results suggest that ALCAR is able to prevent the CCl₄-induced oxidative stress.     

Influence of Selenium on Hepatic Mitochondrial Antioxidant Capacity in Ducklings Intoxicated with Aflatoxin B<Subscript>1</Subscript>

The aim of the study was to investigate the effect of selenium on hepatic mitochondrial antioxidant capacity in ducklings administrated with aflatoxin B₁ (AFB₁). Ninety 7-day-old ducklings were randomly divided into three groups (groups I–III). Group I was used as a blank control. Group II was administered with AFB₁ (0.1 mg/kg body weight). Group III was administered with AFB₁ (0.1 mg/kg body weight) plus selenium (sodium selenite, 1 mg/kg body weight). All treatments were given once daily for 21 days. The results showed that the activities of mitochondrial superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) in group II ducklings significantly decreased when compared with group I (P < 0.01). Furthermore, the content of hepatic mitochondrial malondialdehyde (MDA) significantly increased (P < 0.01). However, the activities of hepatic mitochondrial SOD, CAT, GSH-Px, and GR in group III ducklings significantly increased when compared with group II (P < 0.05). In addition, the content of hepatic mitochondrial MDA significantly decreased (P < 0.01). These results revealed that AFB₁ significantly induced hepatic mitochondrial antioxidant dysfunction. However, sodium selenite could significantly ameliorate the negative effect induced by AFB₁.     

Protective Role of Cactus Cladodes Extract on Sodium Dichromate-Induced Testicular Injury and Oxidative Stress in Rats

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

Effects of Nigella sativa and its Major Constituent, Thymoquinone on Sciatic Nerves in Experimental Diabetic Neuropathy

The aim of this study was designed to investigate the possible beneficial effects of Nigella sativa (NS) and thymoquinone (TQ) on histopathological changes of sciatic nerves in streptozotocin-induced diabetic rats. The rats were randomly allotted into one of four experimental groups: A (control), B (diabetic untreated), C (diabetic treated with NS) and D (diabetic treated with TQ); each group contain ten animals. B, C and D groups received streptozotocin (STZ) to induce diabetes. The rats in NS and TQ treated groups were given NS (in a dose of 400 mg/kg body weight) and TQ (50 mg/kg body weight) once a day orally by using intra-gastric intubation for 12 weeks starting 2 days after STZ injection, respectively. Blood and tissue samples were obtained for biochemical and histopathological investigation. The treatment of both NS and TQ caused a sharp decrease in the elevated serum glucose (P < 0.01, 0.05, respectively), and an increase in the lowered serum insulin concentrations (P < 0.01, 0.05, respectively), in STZ-induced diabetic rats. STZ induced a significant decrease in the area of insulin immunoreactive β-cells (P < 0.0001). NS (P < 0.001) and TQ (P < 0.01) treatment resulted in increased area of insulin immunoreactive β-cells significantly. To date, no histopathological changes of sciatic nerves in STZ induced diabetic rats by NS and TQ treatment have been reported. In this study, histologic evaluation of the tissues in diabetic animals treated with TQ and especially NS showed fewer morphologic alterations. Myelin breakdown decreased significantly after treatment with NS and TQ. The ultrastructural features of axons also showed remarkable improvement. We believe that further preclinical research into the utility of NS and TQ may indicate its usefulness as a potential treatment on peripheral neuropathy (PN) in STZ induced diabetic rats.     

N-Acetyl-L-Cysteine Protects Liver and Kidney Against Chromium(VI)-Induced Oxidative Stress in Mice

Acute hexavalent chromium [Cr(VI)] compound exposure may lead to hepatotoxic and nephrotoxic effects. Cr(VI) reduction may generate reactive intermediates and radicals which might be associated with damage. We investigated effects of N-acetyl-l-cysteine (NAC) pre- or post-treatment on oxidative stress and accumulation of Cr in liver and kidney of Cr(VI)-exposed mice. Intraperitoneal potassium dichromate injection (20 mg Cr/kg) caused a significant elevation of lipid peroxidation in both tissues as compared to control (p < 0.05). Significant decreases in non-protein sulfhydryl (NPSH) level, as well as enzyme activities of catalase (CAT) and superoxide dismutase (SOD) along with significant accumulation of Cr in the tissues (p < 0.05) were of note. NAC pre-treatment (200 mg/kg, ip) provided a noticeable alleviation of lipid peroxidation (p < 0.05) in both tissues, whereas post-treatment exerted significant effect only in kidney. Similarly, Cr(VI)-induced NPSH decline was restored by NAC pre-treatment in both tissues (p < 0.05); however, NAC post-treatment could only replenish NPSH in liver (p < 0.05). Regarding enzyme activities, in liver tissue NAC pre-treatment provided significant restoration on Cr(VI)-induced CAT inhibition (p < 0.05), while SOD enzyme activity was regulated to some extent. In kidney, SOD activity was efficiently restored by both treatments (p < 0.05), whereas CAT enzyme alteration could not be totally relieved. Additionally, NAC pre-treatment in both tissues and post-treatment in liver exerted significant tissue Cr level decreases (p < 0.05). Overall, especially NAC pre-treatment seems to provide beneficial effects in regulating pro-oxidant/antioxidant balance and Cr accumulation caused by Cr(VI) in liver and kidney. This finding may be due to several mechanisms including extracellular reduction or chelation of Cr(VI) by readily available NAC.     

Influence of high inorganic selenium and manganese diets for fattening pigs on oxidative stability and pork quality parameters

Data are scarce regarding combined high Se and Mn supplementation in livestock diets, however, as Se and Mn are functionally related as cofactors of glutathione peroxidase (GPx) and Mn-superoxide dismutase (SOD), respectively, beneficial synergistic effects on oxidative stability of tissues may result. This experiment evaluated the effect of an oversupply of Se and Mn within European legal limits compared with recommendations on performance, oxidative stability of the organism and meat quality in a randomised complete block design. A total of 60 crossbred gilts were fed maize–barley–soya bean meal diets formulated in a 2×2 factorial approach with inorganic Se (0.2 v. 0.5 mg/kg Se dry matter (DM)) or inorganic Mn (20 v. 150 mg/kg Mn DM) from 31 to 116 kg BW. Se supplementation reduced feed intake, whereas high Mn diets impaired average daily gain (P<0.05). Qualitative carcass characteristics were impaired by Se and Mn predominantly in the semimembranosus muscle. Activity of GPx in liver was increased by high Se diets (P<0.05). Mn supplementation increased catalase (CAT) activity in liver, GPx in plasma and total antioxidative capacity (TAC) in muscle, whereas it decreased CAT activity in plasma (P<0.05). Cu/Zn-SOD in muscle showed higher activity in high-Se-low-Mn diets but lower activity when both high Se and Mn were combined (Se×Mn P<0.05). Mn supplementation increased Mn concentration in longissimus thoracis et lumborum, but simultaneously reduced Se concentration (P<0.05). Upon retail display, Mn increased lipid oxidation more pronouncedly (higher thiobarbituric acid reactive substances; P<0.05) than Se (P<0.10). Despite some positive effects (Mn increased TAC, Se increased GPx, Se and Mn increased tenderness), no synergistic effects of high Se and Mn diets or an overall beneficial impact on meat quality, especially during storage, could be observed. Including the negative effects on performance, feeding Se and Mn up to the maximum legal level cannot be recommended.     

Schistosoma mansoni: N-acetylcysteine downregulates oxidative stress and enhances the antischistosomal activity of artemether in mice

Artemether (Art), a derivative of the antimalarial artemisinin, also exhibit antischistosomal properties. N-acetylcysteine (NAC) has a diversity of applications, largely because of the chemical properties of the thiol moiety present in its structure. The ability of this moiety to sweep reactive oxygen species is well-established with NAC. This study investigates the ability of NAC to enhance the therapeutic potential of Art against adult Schistosoma mansoni infection and evaluates the protective role of this antioxidant on S. mansoni-induced oxidative stress. Mice were divided into five groups; normal (i), infected control (ii), infected treated with NAC, 300 mg/kg 5 days a week/4weeks (iii), infected treated with Art (300 mg/kg) 7 weeks post infection (iv) and infected treated with both NAC and Art (v). Results showed that Art produced a significant reduction in total number of worms when used alone. Also, it decreased hepatic ova count significantly accompanied with an increase in the percentage of dead ova. Treatment with NAC alone increased the percentage of dead ova; meanwhile, it enhanced the decrease in total number of worms and hepatic ova count when used with Art. Infection with S. mansoni significantly increased tissue GSH, GR, SOD and serum ALT and GGT, while decreased the activities of GST, GPx and the levels of proteins and albumin compared to normal control. Treatment with NAC alone approximately recovered the contents of GSH, activities of GPx and levels of serum albumin, ALT and GGT relative to normal control. A tendency for normalization in activities of the antioxidant enzymes mentioned above and serum levels of liver function tests was observed in the groups treated with Art alone or Art + NAC. Conclusion: NAC downregulates oxidative stress induced by S. mansoni infection and enhances the therapeutic potential of artemether against adult schistosomes.     

Comparative Analysis of the Protective Effects of Caffeic Acid Phenethyl Ester (CAPE) on Pulmonary Contusion Lung Oxidative Stress and Serum Copper and Zinc Levels in Experimental Rat Model

The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE) in the lungs by biochemical and histopathological analyses in an experimental isolated lung contusion model. Eighty-one male Sprague–Dawley rats were used. The animals were divided randomly into four groups: group 1 (n?=?9) was defined as without contusion and without CAPE injection. Group 2 (n?=?9) was defined as CAPE 10 μmol/kg injection without lung contusion. Group 3 (n?=?36) was defined as contusion without CAPE-administrated group which consisted of four subgroups that were created according to analysis between days?0, 1, 2, and 3. Group 4 (n?=?27) was defined as CAPE 10 μmol/kg administrated after contusion group divided into three subgroups according to analysis on days?1, 2, and 3. CAPE 10 μmol/kg was injected intraperitoneally 30 min after trauma and on days?1 and 2. Blood samples were obtained to measure catalase (CAT) and superoxide dismutase (SOD) activities and level of malondialdehyde (MDA) and for blood gas analysis. Trace elements such as zinc and copper were measured in serum. The lung tissue was also removed for histopathological examination. Isolated lung contusion increased serum and tissue SOD and CAT activities and MDA levels (p?<?0.05). Both serum and tissue SOD, MDA, and CAT levels on day?3 were lower in group 4 compared to group 3 (p?<?0.05). Further, the levels of SOD, MDA, and CAT in group 4 were similar compared to group 1 (p?>?0.05). CAPE also had a significant beneficial effect on blood gases (p?<?0.05). Both serum zinc and copper levels were (p?<?0.05) influenced by the administration of CAPE. Histopathological examination revealed lower scores in group 4 compared to group 3 (p?<?0.05) and no significant differences compared to group 1 (p?>?0.05). CAPE appears to be effective in protecting against severe oxidative stress and tissue damage caused by pulmonary contusion in an experimental setting. Therefore, we conclude that administration of CAPE may be used for a variety of conditions associated with pulmonary contusion. Clinical use of CAPE may have the advantage of prevention of pulmonary contusion.