Can we reduce oxidative stress with liver transplantation?

BackgroundThe aim of this study was to determine the levels of lipid peroxidation (MDA) and antioxidants such as reduced glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) in the blood serum of patients with cirrhosis and liver transplantation.MethodsIn this study, serum malondialdehyde acid (MDA) levels, superoxide dismutase (SOD), reduced glutathione (GSH), and catalase (CAT) activities were measured spectrophotometrically and compared to the results of the healthy control group.ResultsSOD, CAT and GSH activities were significantly decreased in the patient groups compared to the healthy control group (p<0.05). MDA levels were significantly higher in the patient group compared to the healthy control group (p <0.05).ConclusionsIn conclusion, this study demonstrated that oxidative stress may play an important role in the development of liver cirrhosis and in liver transplantation. This study is the first one to show how MDA, SOD, CAT and GSH levels change in liver cirrhosis and liver transplantation, while further studies are essential to investigate antioxidant enzymes and oxidative stress status in patients with cirrhosis and liver transplantation.     

H2O2 at physiological concentrations modulates Leydig cell function inducing oxidative stress and apoptosis

H₂O₂ is one of the active reactive oxygen species secreted by macrophages that are seen closely aligned with Leydig cells in the testicular interstitium. The present study was initiated to investigate the role of H₂O₂ on Leydig cell function in vitro at physiological concentrations. Significant decrease in both testosterone production (p < 0.05) and 3 β-hydroxysteroid dehydrogenase activity (p < 0.05) in adult Leydig cells were observed even with H₂O₂ at low concentrations (30 – 50 μM). H₂O₂ exposure increased oxidative stress in Leydig cells with the rise in lipid peroxidation and fall in the activities of the antioxidant enzymes; superoxide dismutase (SOD), catalase (CAT) & glutathione-s-transferase (GST). There was also a marginal increase (∼8%) in cell apoptosis accompanied by rise in FasL expression and caspase-3 activation. The above findings indicate that H₂O₂ as a bio-molecule modulates Leydig cell function at or below physiological concentrations through a variety of actions like decrease in steroidogenic enzyme activity and increase in oxidative stress and apoptosis.     

Accumulation and oxidative stress biomarkers in Japanese flounder larvae and juveniles under chronic cadmium exposure

This study investigated how Cd exposure affected oxidative biomarkers in Japanese flounder, Paralichthys olivaceus, at early life stages (ELS). Fish were exposed to waterborne Cd (0–48 µg L^− 1) from embryonic to juvenile stages for 80 days. Growth, Cd accumulation, activities of superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6), glutathione S-transferase (GST, EC 2.5.1.18), and levels of glutathione (GSH) and lipid peroxidation (LPO) were investigated at three developmental stages. Flounder growth decreased and Cd accumulation increased with increasing Cd concentration. In metamorphosing larvae, CAT and SOD activities were inhibited and GSH level was elevated, while LPO was enhanced by increasing Cd concentrations. CAT and GST activities of settling larvae were inhibited but GSH level was elevated at high Cd concentrations. In juveniles, SOD activity and LPO level were increased but GST activity was inhibited as Cd concentration increased. Antioxidants in flounder at ELS were able to develop ductile responses to defend against oxidative stress, but LPO fatally occurred due to Cd exposure. These biochemical parameters could be used as effective oxidative biomarkers for evaluating Cd contamination and toxicity in marine environments: CAT, SOD, GSH, and LPO for metamorphosing stage; CAT, GSH, and GST for settling stage; and SOD, GST, and LPO for juvenile stage.     

Response of antioxidant enzymes in rice (<Emphasis Type="Italic">Oryza sauva</Emphasis> L. cv. Dongjin) under mercury stress

We studied the effects of different concentrations of mercury (0.0 to 100 μM) on growth and photosynthetic efficiency in rice plants treated for 21 d. In addition, we investigated how this metal affected the malondialdehyde (MDA) content as well as the activity of five antioxidant enzymes — superoxide dismutase (SOD), ascorbate peroxidase (APX), glutathione reductase (GR), guaiacol peroxidase (POD), and catalase (CAT). Photosynthetic efficiency (Fμ/F_m) and seedling growth decreased as the concentration of Hg was increased in the growth media. Plants also responded to Hg-induced oxidative stress by changing the levels of their antioxidative enzymes. Enhanced lipid peroxidation was observed in both leaves and roots that had been exposed to oxidative stress, with leaves showing higher enzymatic activity. Both SOD and APX activities increased in treatments with up to 50 μM Hg, then decreased at higher concentrations. In the leaves, both CAT and POD activities increased gradually, with CAT levels decreasing at higher concentrations. In the roots, however, CAT activity remained unchanged while that of POD increased a bit more than did the control for concentrations of up to 10 μM Hg. At higher Hg levels, both CAT and POD activities decreased. GR activity increased in leaves exposed to no more than 0.25 μM Hg, then decreased gradually. In contrast, its activity was greatly inhibited in the roots. Based on these results, we suggest that when rice plants are exposed to different concentrations of mercury, their antioxidative enzymes become involved in defense mechanisms against the free radicals that are induced by this stress.     

全氟辛烷磺酸钾对小鼠肾脏的氧化性损伤

目的:以小鼠肾脏细胞中的活性氧(ROS)、丙二醛(MDA)、谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活力为指标,探讨全氟辛烷磺酸钾(PFOS-K)对小鼠肾脏的氧化性损伤作用。方法:以剂量为6mg/kg·bw、12 mg/kg·bw、24 mg/kg·bw 3个浓度的PFOS-K混悬液,每天分别给小鼠经口灌胃一次,连续染毒20天后检测肾脏脏器系数,以及肾脏中ROS、MDA、GSH含量的变化和SOD、GSH-Px、CAT活性的改变。结果:与阴性对照组相比,在6-24 mg/kg·bw剂量范围内,PFOS-K使小鼠体重下降、肾脏重量增加、肾脏脏器系数增大,且表现出一定的剂量-效应关系(r小鼠体重=-0.905,r肾脏湿重=0.938,r脏器系数=0.936)。PFOS-K使小鼠肾脏内活性氧(ROS)及丙二醛(MDA)含量增多(rROS=0.990,rMDA=0.997)、谷胱甘肽(GSH)含量减少(rGSH=-0.994),超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活力降低(rSOD=-0.917,rGSH-Px=-0.986,rCAT=-0.991)。结论:本试验条件下,PFOS-K致使小鼠肾脏肿大,影响了肾脏的发育;造成了肾脏的氧化性损伤,肾组织内抗氧化酶系统遭到破坏,氧化应激反应增强,具有氧化损伤作用。     

Antioxidant enzymes and melatonin levels in patients with bronchial asthma and chronic obstructive pulmonary disease during stable and exacerbation periods

An imbalance between oxidative stress and antioxidative capacity may play an important role in the development and progression of bronchial asthma (BA) and chronic obstructive pulmonary disease (COPD). We carried out a study to assess the systemic oxidant–antioxidant status during the exacerbation and the stable period in patients with BA and COPD. A total of 33 patients, 16 with BA and 17 with COPD were included in the study. During the exacerbation and the stable periods, levels of malondialdehyde (MDA), activities of superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), glutathione reductase (GRd), and catalase (CAT) in erythrocytes and serum melatonin concentrations were investigated. Blood counts, respiratory functions, and blood gases of the patients were also performed. During an exacerbation period of BA, despite the decreases in GSH‐Px, GRd and melatonin levels, MDA and CAT levels, and the white blood cell count, the percentage of eosinophils were significantly higher than in the stable period. Also, it was found that FEV₁/L (where FEV₁ is the forced expiratory volume in 1 s), FVC/L (where FVC is forced vital capacity), PEF/L/s (where PEF is peak expiratory flow), pO₂ (where pO₂ is oxygen pressure) levels increased during the stable period in patients with BA. MDA and SOD values were higher in the exacerbation period than in the stable period although GSH‐Px, GRd, melatonin, pH, and pO₂ values were lower in the exacerbation period than in the stable period. The blood counts and the respiratory function tests did not change between the exacerbation and the stable period of patients with COPD significantly. In conclusion, we observed that oxidative stress in the exacerbation period of patients with BA and COPD increased whereas the antioxidant enzymes and melatonin values reduced. The episodes of BA or COPD might be associated with elevated levels of oxidative stress. Copyright © 2009 John Wiley & Sons, Ltd.     

Butyric acid retention in gingival tissue induces oxidative stress in jugular blood mitochondria

Butyric acid (BA) is a major extracellular metabolite produced by anaerobic periodontopathic bacteria and is commonly deposited in the gingival tissue. BA induces mitochondrial oxidative stress in vitro; however, its effects in vivo were never elucidated. Here, we determined the effects of butyric acid retention in the gingival tissues on oxidative stress induction in the jugular blood mitochondria. We established that BA injected in the rat gingival tissue has prolonged retention in gingival tissues. Blood taken at 0, 60, and 180 min after BA injection was used for further analysis. We isolated blood mitochondria, verified its purity, and measured hydrogen peroxide (H₂O₂), heme, superoxide (SOD), and catalase (CAT) to determine BA effects. We found that H₂O₂, heme, SOD, and CAT levels all increased after BA injection. This would insinuate that mitochondrial oxidative stress was induced ascribable to BA.     

Responses of enzymatic antioxidants and non-enzymatic antioxidants in the cyanobacterium Microcystis aeruginosa to the allelochemical ethyl 2-methyl acetoacetate (EMA) isolated from reed (Phragmites communis)

Macrophytic allelochemicals are considered an environment-friendly and promising alternative to control algal bloom. However, studies examining the potential mechanisms of inhibitory allelochemicals on algae are few. The allelochemical ethyl 2-methyl acetoacetate (EMA), isolated from reed (Phragmites communis), was a strong allelopathic inhibitor on the growth of Microcystis aeruginosa. EMA-induced antioxidant responses were investigated in the cyanobacterium M. aeruginosa to understand the mechanism of EMA inhibition on algal growth. The activities of enzymatic antioxidants superoxide dismutase (SOD) and catalase (CAT), and the contents of non-enzymatic antioxidants reduced glutathione (GSH) and ascorbic acid (AsA) of M. aeruginosa cells were analyzed after treatments with different concentrations of EMA. Exposure of M. aeruginosa to EMA caused changes in enzyme activities and contents of non-enzymatic antioxidants in different manners. The decrease in SOD activity occurred first after 4h of EMA exposure, and more markedly after 40h. CAT activity did not change after 4h of EMA exposure, but increased obviously after 40h. The contents of AsA and GSH were increased greatly by EMA after 4h. After 60h, low EMA concentrations still increased the CAT activity and the contents of AsA and GSH, but high EMA concentrations started to impose a marked suppression on them. EMA increased dehydroascorbate (DHAsA) and oxidized glutathione (GSSG) contents during all exposure times. After 60h, the regeneration rates of AsA and GSH (represented by the AsA/DHAsA ratio and GSH/GSSG ratio, respectively) were reduced by high EMA concentrations. These results suggest that the activation of CAT and the availability of AsA and GSH at early exposure are important to counteract the oxidative stress induced by EMA, and the inactivation of SOD may be crucial to the growth inhibition of M. aeruginosa by EMA.     

山楂叶金丝桃苷对高糖诱导SH-SY5Y细胞损伤的保护作用及机制

为研究金丝桃苷对高糖诱导的人神经母细胞瘤(SH-SY5Y)细胞氧化损伤的保护作用及机制,用含100mmo L/L葡萄糖和分别为20、50、100μmo L/L金丝桃苷的培养基共同孵育SH-SY5Y细胞36 h,检测细胞活力、细胞培养液中乳酸脱氢酶(LDH)水平及半胱氨酸天冬氨酸蛋白酶-3(caspase-3)活性,细胞内活性氧(ROS)水平、丙二醛(MDA)、还原型谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性及SIRT1和NF-кB基因的mRNA水平和蛋白含量。结果显示金丝桃苷可提高高糖诱导后SH-SY5Y细胞的存活率,抑制细胞LDH释放,清除ROS,降低MDA含量与caspase-3活性,增强SOD、CAT活性和GSH含量;同时,金丝桃苷还能提高SIRT1基因的mR-NA表达及蛋白含量,降低NF-кB基因的mRNA水平和蛋白含量。结果表明金丝桃苷能通过激活SIRT1基因,抑制NF-кB基因保护高糖所致SH-SY5Y细胞的氧化损伤。     

Relation between blood levels of heavy metals and some markers of oxidative stress among boys with neuropathic bladder and posterior urethral valve

BackgroundThe status of heavy metals in children with lower urinary tract pathology that may harm the upper tract, e.g., neuropathic bladder and posterior urethral valve and its relationship with oxidative stress has not been adequately investigated. Therefore, the object of the current work was to evaluate the concentrations of copper, zinc, cadmium and lead and their relations with levels of catalase (CAT), malondialdehyde (MDA) and glutathione (GSH) in boys with neuropathic bladder and posterior urethral valve.MethodsThirty-six children with neuropathic bladder, 35 children with posterior urethral valve and 33 health controls were included in the study. In addition to routine laboratory tests, blood samples were collected from patients and controls to assess levels of Cu, Zn, Cd and Pb in addition to plasma concentrations of CAT, MDA and GSH.ResultsSignificantly elevated levels of Cu, Pb, CAT, MDA and GSH and significantly lower concentration of blood Zn were found in the studied groups compared to the controls. In the posterior urethral valve group, blood level of Cu was positively correlated with GSH while a significantly negative relation was observed between blood Zn and CAT activity among the neuropathic bladder patients.ConclusionNeuropathic bladder and posterior urethral valve may lead to abnormalities in the blood levels of heavy metals (i.e. Cu, Pb and Zn) and markers of oxidative stress (CAT, MDA and GSH). Therefore, the levels of theses metal ions should be monitored during the treatment course of neuropathic bladder and posterior urethral valve patients to prevent or minimize long-term oxidative injury.     

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.     

Effect of N‐acetylarginine,a metabolite accumulated in hyperargininemia,on parameters of oxidative stress in rats: protective role of vitamins and L‐NAME

In the present investigation, we initially evaluated the in vitro effect of N‐acetylarginine on thiobarbituric acid‐reactive substances (TBA‐RS), total sulfhydryl content and on the activities of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH‐Px) in the blood, kidney and liver of rats. Results showed that N‐acetylarginine, at a concentration of 5.0 μM, decreased the activity of CAT in erythrocytes, enhanced TBA‐RS in the renal cortex, decreased CAT and SOD activities in the renal medulla and decreased CAT and increased SOD and GSH‐Px activities in the liver of 60‐day‐old rats. Furthermore, we tested the influence of the antioxidants, trolox and ascorbic acid, as well as of the N^ω‐nitro‐L ‐arginine methyl ester (L‐NAME) on the effects elicited by N‐acetylarginine on the parameters tested. Antioxidants and L‐NAME prevented most of the alterations caused by N‐acetylarginine on the oxidative stress parameters evaluated. Data indicate that oxidative stress induction is probably mediated by the generation of NO and/or ONOO^? and other free radicals because L‐NAME and antioxidants prevented the effects caused by N‐acetylarginine in the blood, renal tissues and liver of rats. Our findings lend support to a potential therapeutic strategy for this condition, which may include the use of appropriate antioxidants for ameliorating the damage caused by N‐acetylarginine. Copyright © 2014 John Wiley & Sons, Ltd.     

The effects of boric acid-induced oxidative stress on antioxidant enzymes and survivorship in Galleria mellonella

Larvae of the wax moth, Galleria mellonella (L.), were reared from first instar on a diet supplemented with 156, 620, 1,250, or 2,500 ppm boric acid (BA). The content of malondialdehyde (MDA, an oxidative stress indicator), and activities of the antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glutathione peroxidase (GPx)] were determined in the fat body and hemolymph in the 7th instar larvae and newly emerged pupae. Relative to control larvae, MDA was significantly increased in larval hemolymph, larval and pupal fat body, but decreased in the pupal hemolymph. Insects reared on diets with 156- and 620-ppm BA doses yielded increased SOD activity but 1,250- and 2,500-ppm doses resulted in decreased SOD activity in larval hemolymph. SOD activity was significantly increased but CAT was decreased in the larval fat body. High dietary BA treatments led to significantly decreased GST activity. However, they increased GPx activity in larval hemolymph. Dietary BA also affected larval survival. The 1,250- and 2,500-ppm concentrations led to significantly increased larval and pupal mortality and prolonged development. In contrast, the lowest BA concentration increased longevity and shortened development. We infer that BA toxicity is related, at least in part, to oxidative stress management.     

The organochalcogen 3-methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one induces oxidative stress in heart, liver, and kidney of rats

The objective of this study was to investigate the in vitro effects of the organochalcogen 3-methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one on some parameters of oxidative stress in liver, kidney, and heart of 10-day-old rats. The homogenates of liver, kidney, and heart were incubated for 1 h in the absence (control) or in the presence of 1, 10, or 30 μM of the organoselenium and thiobarbituric acid reactive substances, carbonyl, and the activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were measured. First, we tested the influence of the compound on 1,1-diphenyl-2-picrylhydrazyl (DPPH(?)) radical scavenging and verified that the organochalcogen did not have any antioxidant properties. We observed an increase of lipid peroxidation in all concentrations tested in heart and kidney, while in liver only in the concentrations of 10 and 30 μM. Moreover, we also verified an enhance of protein oxidation in the concentrations of 10 and 30 μM in kidney. On the other hand, the compound caused a reduction on the activity of CAT in heart (10 and 30 μM), liver (30 μM), and kidney (30 μM). The activity of SOD was increased in heart (10 and 30 μM), while in liver (30 μM) and in kidney (10 and 30 μM) the activity was reduced. Our findings indicate that this organoselenium compound induces oxidative stress in liver, heart, and kidney of immature rats, collaborating to the fact that these tissues are potential targets for the organochalcogen action.     

Intraspecific variation in the venom of the vermivorous cone snail Conus vexillum

A combination of proteomic and biochemical assays was used to examine variations in the venom of Conus vexillum taken from two locations (Hurgada and Sharm El-Shaikh) in the Red Sea, Egypt. Using MALDI/TOF-MS, a remarkable degree of intra-species variation between venom samples from both locations was identified. To evaluate variability in the cytotoxic effects of Conus venom, mice were injected with the same dose from each location. The oxidative stress biomarkers [malondialdehyde (MDA), protein carbonyl content (PCC)], antioxidants [glutathione (GSH), superoxide dismutase (SOD), catalase (CAT)], total antioxidant capacity (TAC) and nitric oxide (NO), were measured 3, 6, 9 and 12 h post venom injection. The venoms induced a significant increase in the levels of PCC, MDA, NO, GSH and CAT. The venoms significantly inhibited the activity of SOD and reduced the TAC. Toxicological data showed that the venom obtained from Hurgada was more potent than that obtained from Sharm El-Shaikh. It can be concluded that: (1) the venom of the same Conus species from different regions is highly diversified (2) the venoms from different locations reflect clear differences in venom potency and (3) the cytotoxic effects of C. vexillum venom can be attributed to its ability to induce oxidative stress.     

Time-dependent oxidative stress caused by benznidazole

Abstract

Benznidazole (BZN) is a nitroimidazole derivative which has a notable trypanocide activity, and it is the only drug used in Brazil and Argentina for the treatment of Chagas' disease. The drug in current use is thought to act, at least in part, by inducing oxidative stress within the parasite. Imidazolic compounds are involved in the production of reactive oxygen species (ROS). In order to evaluate the effect of BZN on ROS production and on the antioxidant status of the host, male rats were treated for different periods of time (2, 4, 6, 10 and 30 days) with 40 mg BZN/kg body weight. After treatment, biomarkers of oxidative stress such as the activities of catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST) and glutathione reductase (GR), and also thiobarbituric acid reactive species (TBARS), reduced glutathione (GSH), total glutathione (TG) and oxidized glutathione (GSSG) concentrations, were measured in crude hepatic homogenates. Our results revealed that BZN is able to cause tissue damage as shown by increased TBARS content, inhibition of some antioxidants and induction of other antioxidants in a concentration- and time-dependent manner. The tissue damage measured as TBARS increased up to the 10th day of treatment. GST activity was inhibited during the BZN treatment. On the other hand, CAT and GR showed similar increased activities at the beginning, followed by decreased activities at the end of the treatment. After 30 days of treatment, GR activity remained low while CAT activity was high, compared to controls. The SOD activities remained unchanged throughout the experimental period. GSH showed lower values at the beginning of BZN treatment but the hepatic concentrations were enhanced at the end of the experimental period. Total glutathione showed a similar profile, and oxidized glutathione showed higher values in rats treated with BZN. In conclusion, these results indicate that, at therapeutic doses, BZN treatment elicits an oxidative stress in rat hepatocytes.     

Epicatechin ameliorates ionising radiation-induced oxidative stress in mouse liver

Abstract

The current study was intended to evaluate the hepatoprotective effect of Epicatechin (EC) against radiation-induced oxidative stress, in terms of inflammation and lipid peroxidation. Swiss albino mice were administered with EC (15 mg/kg body weight) for three consecutive days before exposing them to a single dose of 5-Gy ⁶⁰Co gamma (γ) irradiation. Mice were necropsied and livers were taken for immunohistochemistry, western blot analysis and biochemical tests for the detection of markers of hepatic oxidative stress. Nuclear translocation of nuclear factor kappa B (NF-κB) and lipid peroxidation were increased whereas the activities of superoxide dismutase (SOD) and catalase (CAT), reduced glutathione (GSH) content and ferric reducing antioxidant power (FRAP) were diminished upon radiation exposure compared to control. Translocation of NF-κB from cytoplasm to nucleus and lipid peroxidation were found to be inhibited whereas an increase in SOD, CAT, GSH and FRAP was observed in the mice treated with EC prior to irradiation. Thus, pre-treatment with EC offers protection against γ-radiation induced hepatic alterations.     

Metabolic and oxidative impairments in human salivary gland cells line exposed to MeHg

Background/aimThe ingestion of contaminated seafood by MeHg is considered the main route of human exposure, turning the salivary gland one important target organ. The salivary glands play critical roles in maintaining oral health homeostasis, producing saliva that maintains the oral microbiota, initiation of the digestion of macromolecules, and being essential in maintaining the integrity of the adjacent soft tissues and teeth. Thus, this study aimed to investigate the effects of MeHg exposure on human salivary gland cells line.MethodsCells were exposed to 1–6 μM of MeHg for 24 h, and analysis of toxicity was performed. Based on these results, the LC50 was calculated and two concentrations were chosen (0.25 and 2.5 μM MeHg) to evaluate intracellular mercury (Hg) accumulation (THg), metabolic viability and oxidative stress parameters (GSH:GSSG ratio, lipid peroxidation, protein oxidation and DNA damage).ResultsThe results demonstrated accumulation of THg as we increased the MeHg concentrations in the exposure and, the higher the dose, the lower is the cell metabolic response. In addition, the 2.5 μM MeHg concentration also triggered oxidative stress in human salivary gland cells by depleting the antioxidant competence of GSH:GSSG ratio and increasing lipid peroxidation and proteins carbonyl levels, but no damages to DNA integrity.ConclusionIn conclusion, although these two elected doses did not show lethal effects, the highest dose triggered oxidative stress and new questionings about long-term exposure models are raised to investigate furthers cellular damages to human salivary gland cells caused by MeHg exposure to extrapolate in a translational perspective.     

Comparative study of alleviating effects of GSH, Se and Zn under combined contamination of cadmium and chromium in rice (Oryza sativa)

A hydroponic experiment was conducted to study the ameliorative effects of separate or combined application of exogenous glutathione (GSH), selenium (Se) and zinc (Zn) upon 20 μM cadmium (Cd) plus 20 μM chromium (Cr) heavy metal stress (HM) in rice seedlings. The results showed that HM caused a marked reduction in seedling height, chlorophyll content (SPAD) and biomass, and activities of catalase (CAT) and ascorbate peroxidase (APX) in leaves and H⁺-ATPase in roots/leaves, but elevated superoxide dismutase (SOD) and guaiacol peroxidase (POD) activities in leaves with elevated malondialdehyde (MDA) accumulation both in leaves and roots over the control. The best mitigation effect was recorded in HM+GSH+Zn and HM+GSH (addition of GSH+Zn and GSH to HM solution), which greatly alleviated HM-induced growth inhibition and oxidative stress. Compared with HM alone, HM+GSH and HM+GSH+Zn markedly reduced Cr uptake and translocation but not affected Cd concentration; improved H⁺-ATPase activity and Fe, Zn, Mn uptake and translocation, and repressed MDA accumulation. Meanwhile exogenous GSH and GSH+Zn counteracted HM-induced response of antioxidant enzymes, via suppressing HM-induced dramatic increase of root/leaf SOD and leaf POD activities, and elevating stress-depressed leaf APX and leaf/root CAT activities.     

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.