Alterations in Trace Elements and Oxidative Stress in Uremic Patients with Dementia

The present study was conducted to compare the trace elements and oxidative status between uremic patients with and without dementia. Chronic hemodialysis patients with dementia (n = 20) and without dementia (n = 25), and age-matched healthy volunteers (n = 20) were enrolled. The nutritional status, blood levels of trace elements aluminum (Al), zinc (Zn), copper (Cu), magnesium (Mg) and iron (Fe), malondialdehyde (MDA), and protein carbonyl production, antioxidant enzymes glutathione peroxidase (GPx), and glutathione reductase (GR) activities were measured. No significant difference in nutritional status or clinical characteristics was observed between nondementia and dementia patients. However, uremic patients with dementia have significantly higher Al, Cu, and Mg and lower Zn concentrations, as well as increased Cu/Zn ratio in comparison to nondementia patients. There were statistically significant increased MDA and carbonyl production and decreased GPx and GR activities in dementia patients. Furthermore, the significant associations of Al, Mg, and Cu/Zn ratio with oxidative status in patients with dementia were noted. The dementia may initially worsen with abnormal metabolism of trace elements and oxidative stress occurrence. Our results suggest that abnormalities in trace element levels are associated with oxidative stress and may be a major risk factor in the dementia development of uremic patients.     

Parameters related to oxygen free radicals in erythrocytes,plasma and epidermis of the hairless rat

The following parameters related to oxygen free radicals (OFR) were determined in erythrocytes and the epidermis of hairless rats: catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), reduced (GSH) and oxidized (GSSG) glutathione, glutathione S-transferase (GST), superoxide dismutase (SOD) and thiobarbituric acid reactive substances (TBARS). GSH, GSSG and TBARS were also analyzed in plasma. In erythrocytes, the Pearson correlation coefficients (r) were significant (p < 0.001) between glutathione and other parameters as follows: GSH correlated negatively with GSSG (r = -0.665) and TBARS (r = -0.669); GSSG correlated positively with SOD (r = 0.709) and TBARS (r = 0.752). Plasma GSSG correlated negatively with erythrocytic thermostable GST activity (r = -0.608; p=0.001) and with erythrocytic total GST activity (r = -0.677; p < 0.001). In epidermis (p < 0.001 in all cases), GSH content correlated with GSSG (r = 0.682) and with GPx (r = 0.663); GSSG correlated with GPx (r = 0.731) and with GR (r = 0.794). By multiple linear regression analysis some predictor variables (R(2)) were found: in erythrocytes, thermostable GST was predicted by total GST activity and GSSG, GSSG content was predicted by GSH and by the GSH/GSSG ratio and GPx activity was predicted by GST, CAT and SOD activities; in epidermis, GSSG was predicted by GR and SOD activities and GR was predicted by GSSG, TBARS and GPx. It is concluded that the hairless rat is a good model for studying OFR-related parameters simultaneously in blood and skin, and that it may provide valuable information about other animals under oxidative stress.     

Oxidative Damage Induced by Arsenic in Mice or Rats: A Systematic Review and Meta-Analysis

In this meta-analysis, studies reporting arsenic-induced oxidative damage in mouse models were systematically evaluated to provide a scientific understanding of oxidative stress mechanisms associated with arsenic poisoning. Fifty-eight relevant peer-reviewed publications were identified through exhaustive database searching. Oxidative stress indexes assessed included superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), glutathione-s-transferase (GST), glutathione reductase (GR), oxidized glutathione (GSSG), malondialdehyde (MDA), and reactive oxygen species (ROS). Our meta-analysis showed that arsenic exposure generally suppressed measured levels of the antioxidants, SOD, CAT, GSH, GPx, GST, and GR, but increased levels of the oxidants, GSSG, MDA, and ROS. Arsenic valence was important and GR and MDA levels increased to a significantly (P < 0.05) greater extent upon exposure to As³⁺ than to As⁵⁺. Other factors that contributed to a greater overall oxidative effect from arsenic exposure included intervention time, intervention method, dosage, age of animals, and the sample source from which the indexes were estimated. Our meta-analysis effectively summarized a wide range of studies and detected a positive relationship between arsenic exposure and oxidative damage. These data provide a scientific basis for the prevention and treatment of arsenic poisoning.     

Oxidative status and reduced glutathione levels in premature coronary artery disease and coronary artery disease

Identifying patients at risk of developing premature coronary artery disease (PCAD) which occurs at age below 45 years old and constitutes approximately 7–10% of coronary artery disease (CAD) worldwide remains a problem. Oxidative stress has been proposed as a crucial step in the early development of PCAD. This study was conducted to determine the oxidative status of PCAD in comparison to CAD patients. PCAD (<45 years old) and CAD (>60 years old) patients were recruited with age-matched controls (n?=?30, each group). DNA damage score, plasma malondialdehyde (MDA) and protein carbonyl content were measured for oxidative damage markers. Antioxidants such as erythrocyte glutathione (GSH), oxidised glutathione (GSSG), and glutathione peroxidase activity (GPx), superoxide dismutase (SOD) and catalase (CAT) were also determined. DNA damage score and protein carbonyl content were significantly higher in both PCAD and CAD when compared to age-matched controls while MDA level was increased only in PCAD (p<.05). In contrast, GSH, GSH/GSSG ratio, α-tocotrienol isomer, and GPx activity were significantly decreased, but only in PCAD when compared to age-matched controls. The decrease in GSH was associated with PCAD (OR?=?0.569 95%CI [0.375???0.864], p?=?.008) and cut-off values of 6.69?μM with areas under the ROC curves (AUROC) 95%CI: 0.88 [0.80–0.96] (sensitivity of 83.3%; specificity of 80%). However, there were no significant differences in SOD and CAT activities in all groups. A higher level of oxidative stress indicated by elevated MDA levels and low levels of GSH, α-tocotrienol and GPx activity in patients below 45 years old may play a role in the development of PCAD and has potential as biomarkers for PCAD.     

Evaluation of Selenium,Redox Status and Their Association with Plasma Amyloid/Tau in Alzheimer’s Disease

The aim of the study was to evaluate blood selenium and antioxidants as possible oxidative stress markers in Alzheimer’s disease (AD) along with amyloid β42 (Aβ42) and tau by comparing them with vascular dementia (VD) and age-matched healthy controls. Selenium, total tau, Aβ42, glutathione (GSH) and malondialdehyde (MDA) levels and the activities of antioxidant enzymes were analysed in the blood of AD patients (n?=?30), VD patients (n?=?35) and controls (n?=?40) from South India. Plasma Aβ42 level was significantly higher (P?<?0.001) in both AD and VD compared to controls. Total tau and tau-to-amyloid ratio were significantly lower in both AD and VD (P?<?0.001), compared to controls, and a significant difference (P?<?0.01 and P?<?0.05, respectively) was also observed between AD and VD. The receiver operating characteristic (ROC) curve-derived cutoff values of <3.5 for tau-to-Aβ42 ratio and <520 pg/ml for total tau showed sensitivity and specificity of around 67–72 % for differentiating AD from VD and around 90 % for AD from controls, indicating that they could serve as reliable AD-specific markers. The MDA levels were significantly higher (P?<?0.001) in both dementia groups along with a significant decrease (P?<?0.001) in reduced GSH levels, indicating elevated oxidative stress and altered redox status in both forms of dementia. Selenium levels did not vary significantly between the three groups. The activity of glutathione peroxidase increased in both AD and VD compared to controls, with a concomitant decrease in glutathione reductase and glucose-6-phospate dehydrogenase (P?<?0.001) activity. The activity of thioredoxin reductase was significantly lower in both patient groups (P?<?0.001) compared to healthy controls. No correlation was observed between selenium and activities of selenoenzymes, tau, Aβ42 or tau-to-Aβ42 ratio, when analysing independently, indicating that blood selenium may not be directly involved in Aβ production and in regulating tau/Aβ42-mediated mechanism in AD. The present study emphasizes the enhanced oxidative stress in AD pathology and plasma tau and tau-to-amyloid ratio as possible markers to differentiate AD from VD. The study also points that blood selenium may not be involved in regulating oxidative stress in AD, and a longitudinal study correlating plasma and cerebrospinal fluid (CSF) selenium and selenoprotein levels is warranted.     

Depletion of Tip60/Kat5 affects the hepatic antioxidant system in mice

Tat-interactive protein 60 kDa (TIP60, also known as lysine acetyltransferase 5 [KAT5]) is a member of the MYST protein family with histone acetyltransferase activity. Recent studies have reported that TIP60 has multiple functions in many signal transduction mechanisms, especially p53-mediated apoptosis. Although the activation of apoptosis signaling pathways requires the presence of cellular reactive oxygen species (ROS) at a certain level, an imbalance between the production and consumption of ROS in cells results in oxidative stress (OS). In this study, we investigated for the first time how the absence of the Tip60 gene in the liver affects gene expression, enzyme activity, and protein expression of the hepatic antioxidant members localized in the cytoplasm, including superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), and glutathione S-transferase (GST). First, we successfully generated liver-specific Tip60 knockout mice (mutants) using Cre/LoxP recombination. The reduced glutathione level and nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) expression, a marker of OS, increased significantly in the Tip60 mutant liver. Gene expression, activity, and protein expression of the enzymatic antioxidant system, including SOD, CAT, GR, GPx, and GST were investigated in mutants and control groups. Despite a significant correlation between the gene, enzyme activity, and protein content for CAT and GR, this was not true for SOD and GPx. The overall results suggest that TIP60 acts on the hepatic antioxidant system both at the gene and protein levels, but the actual effect of the deletion of Tip60 is observed at the protein level, especially for SOD and GPx.     

Antioxidant enzyme activities and the production of MDA and 8-oxo-dG in chronic lymphocytic leukemia

Chronic lymphocytic leukemia (CLL) is a neoplastic disease susceptible to antioxidant enzyme alterations and oxidative stress. We have examined the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), and the oxidized/reduced glutathione (GSSG/GSH) ratio together with the levels of malondialdehyde (MDA) and 8-oxo-2'-deoxyguanosine (8-oxo-dG) in lymphocytes of CLL patients and compared them with those of normal subjects of the same age. SOD and CAT activity decreased in CLL lymphocytes while GPx activity increased. GSH content of CLL lymphocytes also increased, and GSSG concentration remained constant. Thus, a reduced GSSG/GSH ratio was obtained. The oxidation product MDA, and the damaged DNA base 8-oxo-dG were also increased in CLL. The observed changes in enzyme activities, GSSG/GSH ratio, and MDA were significantly enhanced as the duration of the disease increased in years. The results support a predominant oxidative stress status in CLL lymphocytes and emphasize the role of the examined parameters as markers of the disease evolution.     

The role of Acanthamoeba castellanii (T4 genotype) antioxidant enzymes in parasite survival under H2O2-induced oxidative stress

Acanthamoeba castellanii (A. castellanii) is an important opportunistic parasite. Induction of oxidative stress by the host immune system is one of the most important defense strategies against parasites. Hence, parasites partly deal with oxidative stress by different mechanisms. Identifying resistance mechanisms of A. castellanii parasites against oxidative stress is important to achieve a new therapeutic approach. Thus, this study aimed to understand the resistance mechanisms of A. castellanii, against oxidative stress. Trophozoites of A. castellanii were treated with different concentrations of H₂O₂. The half maximal inhibitory concentration (IC₅₀) of H₂O₂ was determined using the MTT assay. The induction of oxidative stress was confirmed by flow cytometer. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR) were determined. The gene expression levels of CAT and SOD were measured by qRT-PCR. Furthermore, 3-amino-1:2:4-triazole (3-AT) and potassium cyanide (KCN) were used as specific inhibitors of CAT and SOD, respectively. Cell cycle assay and the apoptosis were evaluated by flow cytometer. The activities of SOD, CAT, GR, and GPx, showed an increase in oxidative stress. The cell cycle analysis revealed that most of the cellular population was in G0 and G1 phases. The apoptosis increased in oxidative stress conditions. Moreover, the apoptosis significantly increased after the specific inhibition of CAT and SOD under oxidative stress. The gene expression levels of CAT and SOD significantly increased under oxidative stress. A. castellanii can resist the host immune system through various mechanisms, including evoking its antioxidant enzymes. Therefore, by reducing or inhibiting the activity of the parasite's antioxidant enzymes such as SOD and CAT, it is possible to cope with A. castellanii.     

<Emphasis Type="Italic">Undaria pinnatifida</Emphasis> fucoidan extract protects against CCl<Subscript>4</Subscript>-induced oxidative stress

This study was performed to elucidate the effects of Undaria pinnatifida fucoidan extract (UPFE) in preventing CCl₄-induced oxidative stress. UPFE (100 mg/kg) was intraperitoneally administered to rats for 14 days. On day 15, CCl₄ dissolved in olive oil (50% CCl₄) was injected 12 h before they were anesthetized and dissected. To measure UPFE-mediated antioxidation, we examined the levels of glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) in serum, as well as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in liver homogenates. CCl₄ treatment markedly increased the levels of GOT, GPT, ALP, LDH, and MDA and significantly decreased levels of SOD, CAT, and GPx. UPFE pretreatment decreased levels of GOT, GPT, ALP, LDH, and MDA, by 62.8, 68.5, 41.9, 72.7, and 122%, respectively and increased those of SOD, CAT, and GPx by 111.1, 15.9, and 52.6%, respectively. These results showed that UPFE has antioxidant effects against CCl₄-induced oxidative stress.     

The association between oxidative stress and obstructive lung impairment in patients with COPD

An oxidant/antioxidant imbalance is thought to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). We hypothesized that antioxidant capacity reflected by erythrocyte glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) activities, and serum levels of the lipid peroxidation product malondialdehyde (MDA), may be related to the severity of obstructive lung impairment in patients with COPD. Erythrocyte GPx, SOD and CAT activities, and serum levels of MDA were measured in 79 consecutive patients with stable COPD. Pulmonary functional tests were assessed by body plethysmography. Moderate COPD (FEV1 50-80%) was present in 23, and severe COPD (FEV1 < 50%) in 56 patients. Erythrocyte GPx activity was significantly lower, and serum MDA levels were significantly higher in patients with severe COPD compared to patients with moderate COPD (GPx: 43.1+/-1.5 vs. 47.7+/-2.9 U/gHb, p<0.05, MDA: 2.4+/-0.1 vs. 2.1+/-0.1 nmol/ml, p<0.05). Linear regression analysis revealed a significant direct relationship between FEV1 and erythrocyte GPx activity (r = 0.234, p<0.05), and a significant inverse relationship between FEV1 and serum MDA levels (r = -0.239, p<0.05). However, no differences were observed in the erythrocyte SOD and CAT activities between the two groups of patients with different severity of COPD. Findings of the present study suggest that antioxidant capacity reflected by erythrocyte GPx activity and serum levels of the lipid peroxidation product MDA are linked to the severity of COPD.     

Lead-induced oxidative damage in rats/mice: A meta-analysis

BackgroundLead (Pb) is ubiquitous in the environment and is an environmental genotoxic metal. Pb accumulation in the body could cause the oxidative stress.ObjectiveThis meta-analysis aimed to perform a systematic evaluation of the extent of oxidative damage in rats/mice induced by lead.MethodsAll relevant articles in English or Chinese were retrieved from Embase, PubMed, Web of Science, Medline, China National Knowledge Infrastructure, and Chinese Biological Medicine databases from their inception date until July 22, 2018.ResultsA total of 108 eligible articles were included in this study. The indicators of oxidative stress included malondialdehyde (MDA), glutathione disulfide (GSSG), reactive oxygen species (ROS), hydrogen peroxide (H₂O₂), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), reduced glutathione (GSH), superoxide dismutase (SOD), and glutathione-s-transferase (GST). The meta-analysis showed that lead significantly increased oxidants levels, such as MDA, GSSG, ROS, and H₂O₂ (P < 0.05), and significantly reduced the level of antioxidants, such as CAT, GPx, GR, GSH, SOD, and GST (P < 0.05). The intraperitoneal mode was more effective than water drinking mode in reducing the levels of CAT, GPx, GSH, and SOD (P < 0.05). Other factors that influenced the overall oxidative stress, including species of animals, type of tissues, and intervention dosage and time, were comprehensively evaluated.ConclusionThe results of meta-analysis indicated that mice were more sensitive to lead than rats, and intraperitoneal mode was an effective intervention mean. High doses and long periods of lead treatment can cause serious oxidative damage. Moreover, testicular was more vulnerable to lead than other tissues. These results provided scientific evidence for preventing and treating lead toxicity.     

Benfotiamine Enhances Antioxidant Defenses and Protects against Cisplatin‐Induced DNA Damage in Nephrotoxic Rats

The objective of the present study was to assess superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), paraoxonase (PON1), glutathione reductase (GR), and catalase (CAT) activities ratio and their relationship with DNA oxidative damage in rats treated with cisplatin (3 mg/kg bwt/day) in the presence and absence of benfotiamine (100 mg/kg/day) for 25 days. Cisplatin‐induced renal damage was evidenced by renal dysfunction and elevated oxidative stress markers. SOD activity and levels of nitric oxide, protein carbonyl, malondialdehyde, and 8‐hydroxy‐2'‐deoxyguanosine were significantly increased by cisplatin treatment. Moreover, the ratios of GPx/GR, SOD/GPx, SOD/CAT, and SOD/PON1 were significantly increased compared to control. In contrast, glutathione levels were significantly decreased by cisplatin treatment. Simultaneous treatment of rats with cisplatin and benfotiamine ameliorate these variables to values near to those of control rats. This study suggests that benfotiamine can prevent cisplatin‐induced nephrotoxicity by inhibiting formation reactive species of oxygen and nitrogen. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:398‐405, 2013; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21501     

Differential response to paraquat induced oxidative stress in two rice cultivars on antioxidants and chlorophyll a fluorescence

The responses of antioxidative system and photosystem II photochemistry of rice (Oryza sativa L.) to paraquat induced oxidative stress were investigated in a chilling-tolerant cultivar Xiangnuo no. 1, and a chilling-susceptible cultivar, IR-50. Electrolyte leakage and malondialdehyde (MDA) content of Xiangnuo no. 1 were little affected by paraquat, but they increased in IR-50. After paraquat treatment, superoxide dismutase (SOD) activity remained high in Xiangnuo no. 1, while it declined in IR-50. Activities of catalase (CAT), ascorbate peroxidase (APX) and glutathione reductase (GR) declined with oxidative stress in both cultivars, but Xiangnuo no. 1 had higher GR activity than IR-50. Under paraquat induced oxidative stress, ascorbic acid (AsA) and reduced glutathione (GSH) concentrations remained high in Xiangnuo no. 1, but decreased in IR-50. The results indicated that higher activities of SOD and GR and higher contents of AsA and GSH in Xiangnuo no. 1 under paraquat induced oxidative stress were associated with its tolerance to paraquat, while paraquat induced damage to IR-50 was related to decreased activities of SOD, APX and GR and contents of AsA and GSH. F _v/F _m, Φ _PSII, and qP remained high in Xiangnuo no. 1, while they decreased greatly in IR-50 under paraquat induced oxidative stress.     

Effect of salicylic acid potentiates cadmium-induced oxidative damage in <Emphasis Type="Italic">Oryza sativa</Emphasis> L. leaves

In the present investigation, we studied the possible potentiating effect of salicylic acid (SA) under Cd toxicity in Oryza sativa L. leaves. Cd treatments for 24 h reduced the shoot length, dry biomass and total chlorophyll content followed by high Cd accumulation in shoots. About 16 h presoaking with SA resulted in partial protection against Cd, as observed by minor changes in length, biomass and total chlorophyll. SA priming resulted in low Cd accumulation. Enhanced thiobarbituric acid reactive substances (TBARS), hydrogen peroxide (H₂O₂) and superoxide anion (O₂ ⁻) content were seen when Cd was applied alone, while under SA priming the extent of TBARS, H₂O₂ and O₂ ⁻ were significantly low, suggesting SA-regulated protection against oxidative stress. The antioxidant enzymes like Catalase (CAT), guaiacol peroxidase (GPx), glutathione reductase (GR) and superoxide dismutase (SOD) showed varied activities under Cd alone. CAT activity increased after Cd treatment, followed by a decline in GPX and GR activity. SOD also declined at the highest concentrations with an initial increase. Under SA-priming conditions, the efficiency of the antioxidant enzymes was significantly elevated. GPx and SOD activity showed significant increase in activity. The ascorbate activity increased after Cd treatment, followed by a decline in glutathione under SA-free condition. SA priming showed gradual increase in these non-enzymic antioxidants. Our results indicate that Cd-induced oxidative stress can be regulated by SA.     

Induction of oxidative stress and DNA damage in cervix in acute treatment with benzo[a]pyrene

Benzo[a]pyrene [B(a)P] is one of the most prevalent environmental carcinogens and genotoxic agents. However, the mechanisms of B(a)P-induced oxidative damage in cervical tissue are still not clear. The present study was to investigate the oxidative stress and DNA damage in cervix of ICR female mice induced by acute treatment with B(a)P. Oxidative stress was assayed by analysis of malondialdehyde (MDA), superoxide anion and H(2)O(2), and antioxidant enzymes. The alkaline single-cell electrophoresis (SCGE) was used to measure DNA damage. The contents of MDA and glutathione (GSH), and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST) were significantly increased in cervix 24, 48 and 72h after B(a)P treatment of a single dose of 12.5 and 25mg/kg, while GSH, CAT, SOD and GST had no significant difference with the dose of 50mg/kg B(a)P at post-treatment time 48 and 72h except for SOD activity at 48h which was significant. The maximum values of SOD, CAT, GST and GSH were peaked at 24h and then decreased gradually while GPx activities and MDA levels persisted for up to 72h. Superoxide anion, H(2)O(2) and DNA damage changed similarly as the activity of SOD, CAT or GST. Additionally, increases of formamidopyrimidine DNA glycosylase (FPG) specific DNA damage were observed and can be greatly rescued by vitamin C pretreatment. Overall, B(a)P demonstrated a time- and dose- related oxidative stress and DNA damage in cervix.     

A polysaccharide–peptide complex from abalone mushroom (Pleurotus abalonus) fruiting bodies increases activities and gene expression of antioxidant enzymes and reduces lipid peroxidation in senescence-accelerated mice

The antioxidant effects of a polysaccharide–peptide complex (F22) from mushroom (Pleurotus abalonus)-fruiting bodies were studied. The activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in the liver, kidney, and brain of senescence-accelerated mice showed a marked increase after treatment with the polysaccharide–peptide complex. Concurrently, the gene expression levels of SOD, CAT, and GPx, as determined with real-time polymerase chain reaction, were up-regulated in the liver, kidney, and brain, whereas the MDA content in these organs declined. The maximal lifespan of the mice was prolonged.     

Effects of cadmium exposure on lipid peroxidation and the antioxidant system in fourth-instar larvae of Propsilocerus akamusi (Diptera: Chironomidae) under laboratory conditions

Enzymatic antioxidants such as selenium-dependent glutathione peroxidase (GPx), glutathione transferase (GST), glutathione reductase (GR), and superoxide dismutases (SOD), as well as the concentration of hydrogen peroxide (H2O2) and malondialdehyde (MDA, an indicator of lipid peroxidation) were determined to identify which antioxidant enzymes participate in the efficient scavenging of ROS generated upon exposure to high doses of Cd2+ in fourth-instar Propsilocerus akamusi (Tokuna) (Diptera: Chironomidae) larvae after 72-h exposure. A significant increase in MDA levels and a change in GR and GPx activities in the Cd(2+)-treated P. akamusi were observed. The MDA in 25.0 and 50.0 mmol/liter treatments was significantly higher than that of the control dose after 72 h exposure. GPx activity was significantly induced by Cd2+ exposure only in the 50.0-mmol/liter treatment with a 0.59-fold increase in the control. All doses of Cd2+ significantly suppressed GR activity compared with the findings for the control dose, with an inhibited rate up to 0.55-fold in the 25.0 mmol/liter Cd2+ treatment. SOD and GST activities were not altered. The results indicate that Cd2+ can induce oxidative stress as indicated by the changes in lipid peroxidation and antioxidant status. For P. akamusi, an increase in the dose that the threshold needed for defense (namely, MDA level and GPx activity) activation was achieved. From this, organisms can be hypothesized to enable cells to avoid oxidant stress up to a certain extent where damage is again measurable (higher Cd2+ concentration).     

Fluoride-Induced Oxidative Stress in Rat’s Brain and Its Amelioration by Buffalo (<Emphasis Type="Italic">Bubalus bubalis</Emphasis>) Pineal Proteins and Melatonin

Fluoride (F) becomes toxic at higher doses and induces some adverse effects on various organs, including brain. The mechanisms underlying the neurotoxicity caused by excess fluoride still remain unknown. The aims of this study were to examine F-induced oxidative stress (OS) and role of melatonin (MEL) and buffalo pineal proteins (PP) against possible F-induced OS in brain of rats. The 24 rats were taken in present study and were divided into four groups: control, F, F + PP, and F + MEL. The F group was given 150 mg/L orally for 28 days. Combined 150 ppm F and 100 μg/kg BW (i.p.) PP and F (150 ppm) + MEL (10 mg/kg BW, i.p.) were also administered. The activities of enzymatic, viz., superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione reductase (GR), and non-enzymatic, viz., reduced glutathione (GSH) concentration, and the levels of malondialdehyde (MDA) in the brain tissue were measured to assess the OS. Fluoride administration significantly increased brain MDA compared with control group, while GSH levels were decreased in fluoride-treated groups, accompanied by the markedly reduced SOD, GPx, GR, and SOD activity. Buffalo PP and MEL administration caused brain MDA to decrease but caused SOD, GPx, GR, GSH, and CAT activities to increase to significant levels in F-treated animals. Together, our data provide direct evidence that buffalo PP and MEL may protect fluoride-induced OS in brain of rats through mechanisms involving enhancement of enzymatic and non-enzymatic antioxidant defense system. Therefore, this study suggested that PP and MEL can be useful in control of neurotoxicity induced by fluoride.     

A Comparative Study of the Oxidative Profile in Graves’ Disease, Hashimoto’s Thyroiditis, and Papillary Thyroid Cancer

The aim of this study was to evaluate and compare the oxidative profiles of three thyroid disorders: Graves’ disease (GD), Hashimoto thyroiditis (HT), and papillary thyroid cancer (PTC). Malondialdehyde levels (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activities were examined in the plasma of 52 patients (29 untreated HT, 16 untreated GD, and 7 PTC who underwent surgical therapy). Results were compared with those of 30 healthy controls and among the three groups of patients. The GD, HT, and PTC patients exhibited increased plasma MDA levels and SOD activities compared with the controls (p?<?0.05, p?<?0.05, and p?<?0.001, respectively). CAT activities significantly increased only for the PTC and HT patients (p?<?0.001 and p?<?0.05, respectively), whereas GPx activities significantly decreased only in the GD and PTC (p?<?0.05 and p?<?0.01, respectively). The comparison among the three groups of patients has shown increased MDA level and SOD activity for the PTC patients as compared to the GD patients (p?<?0.01 and p?<?0.001, respectively). Compared with HT, PTC patients exhibited significant higher MDA level, SOD, and CAT activities and a significant lower GPx activity (p?<?0.01, p?<?0.001, p?<?0.05, and p?<?0.05, respectively). No significant discrepancies were noted between the GD and HT patients. Our results have clearly shown an oxidative profile that is highly disturbed for the PTC patients as compared to those of autoimmune disorders. Future studies are needed to determine whether or not the oxidative stress has a prognostic value in this pathology.