Oxidative stress mediated cytotoxicity of TiO2 nano anatase in liver and kidney of Wistar rat

This study examined the adverse effects of TiO₂ nanoparticle (nano-TiO₂) on the kidney and liver of Wistar rats. Changes of serum biochemical parameters and pathological lesions indicated that liver and kidney were significantly affected in animals treated with 50?mg?kg^?1 of nano-TiO₂. The inverse relationship between the level of reactive oxygen species and the activities of superoxide dismutase, catalase, and glutathione peroxidase indicates that nano-TiO₂ induces oxidative stress. A significant increase in the apoptosis of liver and kidney in a dose-dependent manner was also observed. The ultrastructural observations confirmed the internalization of nano-TiO₂ and their direct involvement in the mitochondria-mediated cytotoxicity. Data indicated that nano-TiO₂ induce oxidative stress which produces genotoxicity such as oxidative DNA damage, micronuclei (MN) induction, and cell apoptosis in liver and kidney.     

Evaluation of environmental stress by comet assay on freshwater snail Lymnea luteola L. exposed to titanium dioxide nanoparticles

The use of aquatic organisms to monitor for contamination is well-established. Therefore, this study was designed to assess the adverse effects of titanium dioxide nanoparticles (TiO₂NP) in freshwater snail Lymnea luteola L. (L. luteola). For TiO₂NPs ecotoxicity tests, snails were exposed for seven days. A dose and time-response relationship was observed for TiO₂NP-induced genotoxicity. Induction of oxidative stress in digestive gland was observed by a decrease in glutathione and gluthathions-S-transferase levels accompanied by elevated malondialdehyde levels at TiO₂NP (9 and 28 µg/mL). Superoxide dismutase activities were markedly reduced at TiO₂NP (9 and 28 µg/mL) at days 1 and 3, but not at day 7. Catalase activities were decreased at days 1 and 3 but increased at higher concentration of TiO₂NP at day 7. DNA fragmentation occurring in L. luteola due to ecotoxic impact TiO₂NP was further substantiated by alkaline single-cell gel electrophoresis assay and expressed in terms of percent tail DNA and olive tail moment. The results indicate that the interaction of these TiO₂NP with snail influences the toxicity, which is mediated by oxidative stress in a dose- and time-dependent manner. The measurement of DNA integrity in L. luteola thus provides an early warning signal of contamination of the aquatic ecosystem by TiO₂NP. Data suggest the freshwater snail L. luteola is a potential biomonitor organism.     

铅与纳米SiO2联合染毒对A549细胞氧化损伤的影响

为了研究铅与纳米SiO2联合染毒所致的细胞损伤特征,并从氧化应激方面探讨其可能的作用机制。用铅和SiO2处理A549细胞,采用四唑盐(MTT)比色法检测细胞存活率,评价铅和SiO2联合染毒所致的细胞损伤特征;采用硫代巴比妥酸(TBA)比色法检测细胞内丙二醛(MDA)含量,评价铅与SiO2联合染毒所致细胞的氧化应激状态;检测了细胞内抗氧化物还原型谷胱甘肽(GSH)含量以及细胞内抗氧化酶的活性,以评价铅与SiO2联合染毒对细胞抗氧化系统的影响。将实验数据进行ANOVA分析。结果表明,铅、SiO2单独染毒组各指标没有明显改变;而联合染毒能造成细胞氧化损伤,表现为细胞存活率、GSH水平、超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性显著低于对照组及2个单独染毒组(P<0.05),细胞内MDA含量显著高于对照组及各单独染毒组(P<0.05)。可见,联合染毒可引起明显的细胞毒性,氧化损伤可能是铅与SiO联合染毒致肺细胞毒性损伤的作用机制之一。     

水胺硫磷亚急性暴露对小鼠肝脏氧化应激的影响

为探讨水胺硫磷对小鼠肝脏损伤作用机制,设置0.11、1.08、2.16 mg·kg-13个低、中、高不同剂量组,以灌胃方式对昆明种小鼠进行染毒7 d后,测定小鼠肝脏组织超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)2种抗氧化酶的活性,以及抗氧化物质谷胱甘肽(GSH)和膜脂质过氧化物丙二醛(MDA)含量,同时观察肝脏的组织学变化。结果表明,除低剂量组外,中、高剂量组小鼠肝脏SOD和GSH-Px活性与对照组相比均受到显著抑制(P0.05),GSH的含量与对照组相比显著下降(P0.05),MDA含量与对照组相比却呈显著上升趋势(P0.01),同时各指标的变化均呈一定的剂量-效应关系。组织学观察显示中、高剂量组肝细胞出现明显水肿和坏死,肝窦狭窄甚至闭塞。结果表明氧化损伤可能是水胺硫磷致小鼠肝脏毒性损伤的作用机制之一。     

纳米TiO2与重金属Cd对铜绿微囊藻生物效应的影响

为了更全面地评价纳米TiO2的生物效应,尤其是纳米TiO2与其他环境污染物的联合作用,以铜绿微囊藻为受试生物,探讨了不同浓度的纳米TiO2,以及纳米TiO2与Cd联合作用对藻生长的影响。根据叶绿素a及藻胆蛋白的含量变化,低浓度的纳米TiO2溶液(0～50mg.L-1)可以促进藻的生长,当纳米TiO2的浓度大于50mg·L-1时,藻细胞的生长有所抑制,生长减慢,并呈剂量-效应关系;当纳米TiO2与Cd离子同时存在时,由于纳米TiO2对Cd离子的吸附作用,水中游离态Cd离子浓度降低,Cd离子对藻的毒性明显降低。因此,纳米TiO2的生态毒性和环境效应不容忽视,同时,应重视纳米材料及与其他环境污染物质共同作用后的生物效应。     

Dichloroacetate- and trichloroacetate-induced modulation of superoxide dismutase,catalase, and glutathione peroxidase activities and glutathione level in the livers of mice after subacute and subchronic exposures

Dichloroacetate (DCA) and trichloroacetate (TCA) were previously found to induce various levels of oxidative stress in the hepatic tissues of mice after subacute and subchronic exposures. The cells are known to have several protective mechanisms against production of oxidative stress by different xenobiotics. To assess the roles of the antioxidant enzymes and glutathione (GSH) in DCA- and TCA-induced oxidative stress, groups of B6C3F1 mice were administered either DCA or TCA at doses of 7.7, 77, 154, and 410 mg kg^?1 day^?1, by gavage for 4 weeks (4-W) and 13 weeks (13-W), and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as GSH were determined in the hepatic tissues. DCA at doses ranging between 7.7–410, and 7.7–77 mg kg^?1 day^?1, given for 4-W and 13-W, respectively, resulted in either suppression or no change in SOD, CAT, and GSH-Px activities, but doses of 154–410 mg DCA kg^?1 day^?1 administered for 13-W were found to result in a significant induction of the three enzyme activities. TCA administration on the other hand, resulted in increases in the SOD and CAT activities, but caused suppression of GSH-Px activity in both the periods. Except for the DCA doses of 77–154 mg kg^?1 day^?1 administered for 13-W that resulted in a significant reduction in the GSH levels, all other DCA as well as TCA treatments produced no changes in GSH. Since these enzymes are involved in the detoxification of the reactive oxygen species (ROS), superoxide anion (SA), and H₂O₂, it is concluded that SA is the main contributor to DCA-induced oxidative stress, while both ROS contribute to that of TCA. The increase in the enzyme activities associated with 154–410 mg DCA kg^1? day^?1 in the 13-W period suggest their role as protective mechanisms contributing to the survival of cells modified in response to those treatments.     

Tualang honey supplementation improves oxidative stress status among chronic smokers

Free radicals induced by cigarette smoking have been linked to an increase in oxidative stress resulting in smoking-related cardiovascular diseases. However, the possible effect of honey that has antioxidant property in improving oxidative stress status among smokers has not yet been reported. Hence, this study was to determine the effects of 12-week Tualang honey supplementation on F₂-isoprostanes, superoxide dismutase, glutathione peroxidase, catalase, and total antioxidant status among chronic smokers. A total of 32 non-smokers and 64 chronic smokers were recruited from Quit Smoking Clinic and Health Campus, Universiti Sains, Malaysia. Smokers were randomized into two groups (n = 32/group) namely smokers without supplementation and smokers with honey supplementation (20 g/day) for 12 weeks. Blood was obtained from non-smokers and smokers at pre-intervention and from smokers at post-intervention. During pre-intervention, the levels/activity of F₂-isoprostanes, total antioxidant status, and catalase were significantly higher while superoxide dismutase and glutathione peroxidase were lower in smokers than non-smokers. During post-intervention, in supplemented smokers, there were significant decrease in F₂-isoprostanes and increase in total antioxidant status, glutathione peroxidase and catalase levels/activities compared with pre-intervention. This study indicates that honey supplementation improves oxidative stress status suggesting a beneficial role of honey in reducing the risk of cardiovascular diseases.     

The ecotoxicology of titanium dioxide nanoparticles,an important engineering nanomaterial

Abstract

Titanium dioxide nanoparticles (nano-TiO₂) are useful because of their unique physicochemical properties. The wide application of nano-TiO₂ has raised concerns regarding its potential threat to organisms and the environment. Therefore, the production and application of nano-TiO₂ in the global market is summarized in this paper. This review presents the adverse effects of nano-TiO₂ in vivo, including potential exposure routes such as transdermal, oral and inhalative exposure, risk evaluation of nanotoxicity in vitro using bacteria, microorganisms, cells and biological molecules), physicochemical characterization of nano-TiO₂ regarding crystal structure, size, shape, surface characteristics and coatings, and the mechanisms of toxicity of nano-TiO₂ based on environmentally relevant test species and cells. This review aims to fill deficiencies in toxicological research and to facilitate the assessment of the environmental risks by nano-TiO₂ which is conducive to designing safer nanoproducts in our daily life.

• Highlights

• Presented the possible human health hazards related to nano-TiO2 exposure.

• Identified the current research deficiencies in this area.

• Summarized the underlying toxicity mechanisms.

• Summarized the compound toxicity of NPs.

     

Seed pre-soaking with 24-epibrassinolide reduces the imidacloprid pesticide residues in green pods of Brassica juncea L.

The effect of 24-epibrassinolide seed soaking on imidacloprid residues in green pods and mature seeds of Brassica juncea L. plants was investigated. The activities of the antioxidative enzymes glutathione-S-transferase, glutathione peroxidase, glutathione reductase, ascorbate peroxidase and guaiacol peroxidase, and the content of glutathione were determined. Imidacloprid residues in green pods were analyzed and quantified by gas chromatography-mass spectrometry, revealing that 24-epibrassinolide treatment resulted in a decrease of residues by almost 30%. In mature seeds, no pesticide residues were detected. Activities of all the antioxidative enzymes and glutathione content were found to be high in plants grown in soil amended with 300 mg imidacloprid kg^?1 soil, but pre-soaking with 100 nmol L^?1 24-epibrassinolide further enhanced the activities of all these enzymes and the glutathione content.     

Effects of arsenic on reactive oxygen species and antioxidant defense system in tomato plants

In this study, the generation of reactive oxygen species, the induction of oxidative stress, and the response of the antioxidative system in hydroponically grown tomato plants as the cause of arsenic-induced phytotoxicity are investigated. Reduction in plant growth was measured in terms of dry weight and length of roots and shoots, the latter accumulating more arsenic than the roots. The treatment resulted in increased formation of superoxide anion (O₂^.?), H₂O₂, and thiobarbituric acid reactive substances, which indicate augmented lipid peroxidation. Superoxide dismutase, catalase (CAT), and ascorbate peroxidase activities were increased in arsenic-treated tomato plants while CAT activity was insignificantly increased.     

Effects of Matricaria chamomilla L. on lipid peroxidation,antioxidant enzyme systems,and key liver enzymes in CCl4-treated rats

In this study, we investigated the effects of Matricaria chamomilla L. extract (MCE) on lipid peroxidation, antioxidant enzyme systems, and several liver enzymes in carbon tetrachloride (CCl₄)-treated rats. Rats were divided into five groups. The first group (control group) was fed on standard feed. The rats in the other groups (CCl₄, MCE50, MCE100, and MCE200) were injected intraperitoneally with 0.8?mL?kg^?1 CCl₄. Moreover, rats in the MCE50, MCE100, and MCE200 groups were gavaged with 50?mg?kg^?1, 100?mg?kg^?1, and 200?mg?kg^?1 MCE, respectively. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, whole blood malondialdehyde (MDA) and glutathione (GSH) levels, and erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activity levels were measured after 14 days of exposure. ALT and AST in the CCl₄ group increased significantly in comparison to the control group (p?4, MCE50, MCE100, and MCE200 groups at different significance levels. In conclusion, the findings suggest that, depending on the dose administered, MCE decreases CCl₄-induced damage and consequent oxidative stress in rats; it affects the antioxidant system positively.     

Preparation and characterization of poly (vinylidene fluoride)/TiO2 hybrid membranes

Poly(vinylidene fluoride) (PVDF)/titanium dioxide (TiO₂) hybrid membranes were prepared using nano-TiO₂ as the modifier, and characterized by Transmission Electron Microscope (TEM), Fourier transform infrared spectroscopy (FT-IR), scanning electron microscope (SEM), atomic force microscope (AFM), X-ray diffraction (XRD) and X-ray photoelectron spectroscopy (XPS). The characterization results demonstrated that nano-sized TiO₂ particles dispersed homogeneously within the PVDF matrix, contributing to more hydroxyls and smoother surfaces. Moreover, permeate flux, retention factor, porosity, contact angle and anti-fouling tests were carried out to evaluate the effect of TiO₂ concentration on the performance of PVDF membranes. Among all the prepared membranes, PVDF/TiO₂ membrane containing 10 vol.% TiO₂ exhibited the best hydrophilicity with an average pure water flux up to 237 L·m^?2·h^?1, higher than that of unmodified PVDF membranes (155 L·m^?2·h^?1). Besides, the bovine serum albumin rejection of the hybrid membrane was improved evidently from 52.3% to 70.6%, and the contact angle was significantly lowered from 83° to 60°, while the average pore size and its distribution became smaller and narrower.     

Antioxidant enzymatic activities and lipid peroxidation in liver and ovary of zebrafish (Danio rerio) exposed to deltamethrin

Deltamethrin (DM) is being used as a substitute for organochlorines and organophosphates in pest control because of its low environmental persistence and toxicity. But it has become an environmental contaminant as it has been used widely. In this study, we investigated the effect of DM (technical grade) on the antioxidant system of adult zebrafish. For this, six-month-old fish were exposed to 2, 4 and 6?μg/L of DM for 96?h. The tissues selected were liver and ovary. Our data showed that exposure to DM increases CAT (catalase), SOD (superoxide dismutase), GPx (glutathione peroxidase, antioxidant enzymes), LPO (lipid peroxidation, non-enzymatic antioxidant) and GST (glutathione S-transferase, detoxifying enzyme) in liver and ovary. Increased GST could detoxify the toxicant; still there could be enough DM to cause oxidative stress. It appears from our study that zebrafish used compensatory mechanisms in eliminating reactive oxygen species. These data will be useful as oxidative stress is being used as a biomarker for aquatic pollution.     

镧、铈、钕对小鼠肝细胞核的氧化损伤作用

轻稀土元素进入生物体后主要累积于肝脏,进入肝细胞,分布于细胞核上.为探讨轻稀土元素对小鼠肝细胞核的氧化损伤作用,选用5周龄雄性封闭群(ICR)小鼠灌喂10、20和40 mg·kg-1的稀土元素镧(La)、铈(Ce)和钕(Nd),6周后测定小鼠肝细胞核中超氧化物岐化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(...     

Effect of latex material on antioxidant enzymes,lipid peroxidation,DNA damage,and chromosomal aberration

Cell integrity is affected by oxidative stress when the production of active oxidants overwhelms antioxidant defense mechanisms. Latex, a natural polymer obtained from Hevea brasiliensis, is used in medical industry for manufacturing surgical gloves, urinary catheters, and dental dams. The aim of this study was to evaluate the effects of latex material on oxidative stress by in vivo and in vitro methods. In addition, the material was screened for its ability to induce any chromosomal aberrations (CAs) by in vitro method. In vivo studies were carried out with implanted latex material onto subcutaneous tissue of various batches of experimental Wistar rats. At the end of experimental period, animals were anesthetized, blood was collected for serum analysis, and sacrificed. Liver was excised for the determination of antioxidant enzymes and lipid peroxidation (LPO). Subcutaneous tissues were obtained for the extraction of genomic DNA from implanted animals and checked for the presence of 8-hydroxy-2-deoxyguanosine (8-OHdG), considered an indicator of DNA damage. Simultaneously, in vitro studies were carried out using fresh liver and subcutaneous tissue obtained from Swiss albino mice treated with physiological saline extract of latex material. For the estimation of both in vitro and in vivo oxidative stress, 10% liver homogenate was assessed for stress indicators like reduced glutathione, glutathione reductase, glutathione peroxidase, LPO and protein content. The results of both in vivo and in vitro studies indicated that the chemical leachents from the latex material did not significantly affect LPO and the levels of antioxidant enzymes. There was also no significant increase in 8-OHdG content due to the presence of implanted latex material. Finally, the results of in vitro CA test and G banding indicated that extracts of test material did not induce any chromosomal abnormalities.     

Photocatalytic mineralization of a water pollutant,Sunset Yellow dye by an advanced oxidation process using a modified catalyst

ZnS-loaded TiO₂ (ZnS–TiO₂) was synthesized by a sol–gel method. The catalyst was characterized by using different techniques (XRD, HR-SEM, EDS, DRS, PL, XPS, and BET methods). The photocatalytic activity of ZnS–TiO₂ was investigated for the degradation of Sunset Yellow FCF (SY) dye in an aqueous solution using ultraviolet light. ZnS–TiO₂ is found to be more efficient than prepared TiO₂, TiO₂–P25, TiO₂ (Merck), and ZnS at pH 7 for the mineralization of SY. The effects of operational parameters such as the amount of photocatalyst, dye concentration, and initial pH on photo mineralization of SY have been analyzed. The mineralization of SY has been confirmed by chemical oxygen demand measurements. The catalyst is found to be reusable.     

Involvement of mitochondrial-mediated caspase-3 activation and lysosomal labilization in acrylamide-induced liver toxicity

Acrylamide (ACR) is a chemical frequently used in both industrial and synthetic processes and may be produced during food processing. ACR at very high concentrations is postulated to exert its toxicity through the stimulation of an oxidative stress. ACR in excessive doses induces the central nervous system, reproduction, and genetic toxicity. However, ACR effects on the liver, a major organ of drug metabolism, have not been adequately explored. In addition, the role of mitochondria in an ACR-mediated hepatotoxicity is still unclear. The aim of this study was to investigate the cytotoxic mechanisms attributed to ACR using isolated rat hepatocytes. Hepatocytes were isolated by the collagenase perfusion method and incubated with an EC50_2hr concentration of ACR for 3 hr. The EC50_{2 hr} of ACR on isolated rat hepatocytes was determined to be 1 mM. Based on our results, hepatocytes cytotoxicity of ACR (1 mM) was mediated by a reactive oxygen species formation and lipid peroxidation. Incubation of hepatocytes with ACR produced rapid hepatocyte glutathione depletion which is another marker of the cellular oxidative stress. ACR cytotoxicity was also associated with mitochondrial injury as evidenced by the decline of mitochondrial membrane potential and lysosomal membrane leakiness. Our results also showed that ACR induced caspase-3 activation, the final mediator of apoptosis signaling. These findings contribute to a better understanding underlying mechanisms involved in ACR hepatotoxicity originating from the oxidative stress and ending in mitochondrial/lysosomal damage and cell death signaling.     

Mercuric chloride induced proteotoxicity and structural destabilization in marine fish (Therapon jarbua)

The reaction byproducts derived from lipid peroxidation (LPO), as well as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) enzyme activities were measured in tissues of marine fish (Therapon jarbua) exposed to mercuric chloride (HgCl) in water dispersions of 0.125 or 0.25 ppm. LPO was significantly increased in various tissues relative to control values after 96-h exposure. SOD and GPx activities significantly decreased after exposure to first two doses but significantly elevated CAT in Dose II kidney and liver tissues. The elevated levels of LPO, decreased activities of SOD and GPx, and increased CAT activities in all tissues examined in T. jarbua are an index of oxidative stress in fish. Structural analysis by scanning electron microscopy studies revealed the structural deformation in HgCl₂-exposed animals. These observations suggest that HgCl acts as a mediator in free radical generation. The increase in CAT and decrease in SOD and GPx activities in these tissues may be an adaptive response.     

PM_(2.5)和甲醛联合暴露致小鼠肺损伤及其分子机制的研究

我国城市当前普遍存在室外大气PM_(2.5)与室内甲醛(FA)联合污染状况,二者均被报道在单独暴露下可以导致肺损伤并诱导和诱发哮喘的急性发作,但其联合污染的具体效应,以及分子机制目前尚不清楚。为探究PM_(2.5)和/或甲醛暴露对小鼠的肺损伤及其可能的机制,分别将雄性Balb/c小鼠分为以下6组:对照组,AZD8055组,PM_(2.5)组,FA组,PM_(2.5)+FA组,PM_(2.5)+FA+AZD8055组。染毒结束后,观察肺组织病理学变化;检测肺组织氧化损伤,活性氧(reactive oxygen species,ROS),还原型谷胱甘肽(glutathione,GSH)和丙二醛(malondialdehyde,MDA)的含量,DNA损伤,DNA-蛋白质交联(DNA-protein crosslink,DPC)系数和8羟基脱氧鸟苷(8-OH-d G)的含量,以及细胞凋亡、半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)的含量。结果表明,当吸入气态甲醛浓度为3 mg·m-3,气道滴注PM_(2.5)浓度为2.5 mg·m L-1时,肺组织出现不同程度的支气管重塑和炎症细胞浸润。ROS显著上升,GSH显著下降,DPC、8-OH-d G以及Caspase-3都显著上升。添加AZD8055后,肺组织损伤效应更加显著。PM_(2.5)复合甲醛的暴露导致小鼠肺损伤具有协同作用,氧化应激及其下游的DNA损伤可能是甲醛联合PM_(2.5)致小鼠肺损伤的一种重要机制。     

Cytotoxicity and cell membrane depolarization induced by aluminum oxide nanoparticles in human lung epithelial cells A549

The cytotoxicity of 13 and 22 nm aluminum oxide (Al₂O₃) nanoparticles was investigated in cultured human bronchoalveolar carcinoma-derived cells (A549) and compared with 20 nm CeO₂ and 40 nm TiO₂ nanoparticles as positive and negative control, respectively. Exposure to both Al₂O₃ nanoparticles for 24 h at 10 and 25 µg mL^?1 doses significantly decreased cell viability compared with control. However, the cytotoxicity of 13 and 22 nm Al₂O₃ nanoparticles had no difference at 5–25 µg mL^?1 dose range. The cytotoxicity of both Al₂O₃ nanoparticles were higher than negative control TiO₂ nanoparticles but lower than positive control CeO₂ nanoparticles (TiO₂ < Al₂O₃ < CeO₂). A real-time single cell imaging system was employed to study the cell membrane potential change caused by Al₂O₃ and CeO₂ nanoparticles using a membrane potential sensitive fluorescent probe DiBAC₄(3). Exposure to the 13 nm Al₂O₃ nanoparticles resulted in more significant depolarization than the 30 nm Al₂O₃ particles. On the other hand, the 20 nm CeO₂ particles, the most toxic, caused less significant depolarization than both the 13 and 22 nm Al₂O₃. Factors such as exposure duration, surface chemistry, and other mechanisms may contribute differently between cytotoxicity and membrane depolarization.