Acetylcysteine ; pharmacology ; Antioxidants ; pharmacology ; Composite Resins ; toxicity ; Dental Materials ; toxicity ; Fibroblasts ; drug effects ; metabolism ; Gingiva ; cytology ; drug effects ; Humans ; Methacrylates ; toxicity ; Polyethylene Glycols ; toxicity ; Polymethacrylic Acids ; toxicity ; Polymethyl Methacrylate ; toxicity ; Reactive Oxygen Species ; metabolism ; Resins, Synthetic ; toxicity

This study aimed to investigate the neurotoxicity induced by trichloroacetic acid (TCA) and the possible protective mechanisms of boron (B). Mouse BV2 cells were treated with TCA (0, 0.39, 0.78, 1.56, 3.12, 6.25, or 12.5 mmol/L) and B (0, 7.8, 15.6, 31.25, 62.5, 125, 500, or 1,000 mmol/L) for 3 h and 24 h, respectively. Then, reactive oxygen species, and supernatant proinflammatory cytokine and protein levels were analyzed after 24 h of combined exposure. Beyond the dose-dependent decrease in the cellular viability, it clearly increased after B supplementation ( P < 0.05). Moreover, B decreased oxidative damage, and significantly down-regulated IL-6 levels and up-regulated TNF-β production ( P < 0.05). B also decreased apoptosis via the p53 pathway. The present findings indicated that TCA may induce oxidative damage, whereas B mitigates these adverse effects by decreasing cell apoptosis.
Animals ; Apoptosis ; Boron/toxicity* ; Mice ; Oxidative Stress ; Reactive Oxygen Species/metabolism* ; Trichloroacetic Acid/toxicity* ; Tumor Suppressor Protein p53/metabolism*

OBJECTIVETo measure the toxicity of phenol, aniline, and their derivatives to algae and to assess, model, and predict the toxicity using quantitative structure-activity relationship (QSAR) method.

METHODSOxygen production was used as the response endpoint for assessing the toxic effects of chemicals on algal photosynthesis. The energy of the lowest unoccupied molecular orbital (E(LUMO)) and the energy of the highest occupied molecular orbital (E(HOMO)) were obtained from the ChemOffice 2004 program using the quantum chemical method MOPAC, and the frontier orbital energy gap (deltaE) was obtained.

RESULTSThe compounds exhibited a reasonably wide range of algal toxicity. The most toxic compound was alpha-naphthol, whereas the least toxic one was aniline. A two-descriptor model was derived from the algal toxicity and structural parameters: log1/EC50 = 0.268,logKow - 1.006deltaE + 11.769 (n = 20, r2 = 0.946). This model was stable and satisfactory for predicting toxicity. CONCLUSION Phenol, aniline, and their derivatives are polar narcotics. Their toxicity is greater than estimated by hydrophobicity only, and addition of the frontier orbital energy gap deltaE can significantly improve the prediction of logKow-dependent models.

Aniline Compounds ; toxicity ; Oxygen ; metabolism ; Phenols ; toxicity ; Photosynthesis ; drug effects ; Quantitative Structure-Activity Relationship ; Scenedesmus ; drug effects ; metabolism ; Water Pollutants, Chemical ; toxicity

OBJECTIVESTo analyze the changes of movement function and viability in human spermatozoa induced by reactive oxygen species(ROS), and to prove whether ROS were one of the causes of the movement dysfunction of spermatozoa.

METHODSSpermatozoa with normal physiological functions selected from semen samples by Percoll gradient centrifugation technique were regarded as normal sperm models. ROS were generated by hypoxanthine-xanthine oxidase system and then incubated with normal sperm models under aerobic environment. After model spermatozoa were incubated with ROS, movement parameters of spermatozoa were analyzed by computer-assisted semen analysis (CASA) system.

RESULTSCompared with the control group, after model spermatozoa were incubated with ROS for 30 minutes, motility, curvilinear velocity(VCL), straight line velocity (VSL) and average path velocity (VAP) of the spermatozoa were significantly decreased (P < 0.001), but amplitude of lateral head displacement (ALH) was insignificant (P > 0.05). When incubated with ROS for 60 minutes, spermatozoa almost lost movement function and all movement parameters of spermatozoa inclined to zero.

CONCLUSIONSWhen normal spermatozoa were incubated with ROS, movement functions of sperm were decreased. It was demonstrated that ROS were one of the causes of the movement dysfunction of spermatozoa.

Adult ; Cell Survival ; drug effects ; Humans ; Male ; Reactive Oxygen Species ; toxicity ; Sperm Motility ; drug effects

OBJECTIVE: Mitophagy is known to contribute towards progression of Parkinson's disease. Korean red ginseng (KRG) is a widely used medicinal herb in East Asia, and recent studies have reported that KRG prevents 1-methyl-4-phenylpyridinium ion (MPP METHODS: SH-SY5Y cells were incubated with KRG for 24 h, and subsequently exposed to MPP RESULTS: MPP CONCLUSION KRG effectively prevents MPP
1-Methyl-4-phenylpyridinium/toxicity* ; Apoptosis ; Cell Line, Tumor ; Mitochondria ; Mitophagy ; Panax ; Reactive Oxygen Species

BACKGROUND: Pulmonary damage resulting from lipid peroxidation is a principal effect of paraquat intoxication. The host-defense functions of surfactant are known to be mediated by the surfactant proteins A and D (SP-A and SP-D, respectively). The primary objective of this study was to evaluate the variations over time in levels of surfactant protein and lipid peroxidation (LPO) in lung tissue following free-radical-induced injury. METHODS: 42 adult, male, Sprague-Dawley rats were administered intraperitoneal injections of paraquat (35 mg/kg body weight). SP-A and SP-D levels were determined via Western blot. LPO in the left lung homogenate was measured via analyses of the levels of thiobarbituric acid-reactive substances. RESULTS: LPO levels peaked at 6 hours, with no associated histological changes. SP-D levels increased until hour 12 and declined until hour 48; SP-D levels subsequently began to increase again, peaking at hour 72. SP-A levels peaked at hour 6, declining thereafter. CONCLUSIONS: We suggest that in the early phase of paraquat injury, SP-D levels reflect alveolar damage and that de novo synthesis of SP-D takes 72 hours. Levels of SP-A, on the other hand, reflect abnormalities in the surfactant system in the late stage of paraquat intoxication. Surfactant proteins may play a role in protecting the lungs from reactive oxygen injury. A time-dependent variation has been observed in the levels of surfactant proteins A and D following paraquat injury, and it has been suggested that these proteins play a role in the protection of lung tissue against ROS-induced injuries.
Animals ; Free Radicals/*toxicity ; Herbicides/*toxicity ; *Lipid Peroxidation ; Lung/*drug effects ; Male ; Paraquat/*toxicity ; Pulmonary Surfactant-Associated Proteins/*analysis ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/toxicity ; Respiratory Distress Syndrome, Adult/*chemically induced

OBJECTIVETo investigate the toxic effects of decabromodiphenyl ethane (DBDPE), used as an alternative to decabromodiphenyl ether in vitro.

METHODSHepG2 cells were cultured in the presence of DBDPE at various concentrations (3.125-100.0 mg/L) for 24, 48, and 72 h respectively and the toxic effect of DBDPE was studied.

RESULTSAs evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and lactate dehydrogenase assays and nuclear morphological changes, DBDPE inhibited HepG2 viability in a time- and dose-dependent manner within a range of 12.5 mg/L to 100 mg/L and for 48 h and 72 h. Induction of apoptosis was detected at 12.5-100 mg/L at 48 h and 72 h by propidium iodide staining, accompanied with overproduction of reactive oxygen species (ROS). Furthermore, N-acetyl-L-cysteine, a widely used ROS scavenger, significantly reduced DBDPE-induced ROS levels and increased HepG2 cells viability.

CONCLUSIONDBDPE has cytotoxic and anti-proliferation effect and can induce apoptosis in which ROS plays an important role.

Apoptosis ; drug effects ; Bromobenzenes ; toxicity ; Cell Survival ; drug effects ; Dose-Response Relationship, Drug ; Environmental Pollutants ; toxicity ; Hep G2 Cells ; Humans ; Reactive Oxygen Species ; Time Factors

OBJECTIVETo explore the effects of chronic exposure to trace chromium (VI) as a result of metal-on-metal hip arthroplasty on oxidative stress in mouse liver cells.

METHODSEighty NIH mice were randomly divided into 4 groups and subject to intraperitoneal injection of CrO(3) at the dose of 0, 5, 10 or 20 mg/kg every other day for 16 weeks. Five mice from each group were selected every 4 weeks for determining the content of chromium (VI) in the whole blood and the levels of reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), glutathione reductase (GR) activity, and glutamate cysteine ligase (GCL) expression in the liver cells. The ultrastructural changes of the liver cells were also observed using transmission electron microscopy.

RESULTSExposure to 5 and 10 mg/kg CrO(3) caused significantly increased blood chromium concentration and ROS level, which reached the peak level at 8 weeks and became stabilized, whereas at the dose of 20 mg/kg, CrO(3) exposure resulted in progressive, time-dependent increase of blood chromium concentration and ROS level. MDA showed no significant changes in the 4 groups. With the prolongation of the exposure time, GSH content and GR activity were decreased in these groups. In 5 and 10 mg/kg CrO(3) groups, GCL expression increased at each time point of measurement, but in 20 mg/kg group, GCL expression decreased gradually with a prolonged exposure. Transmission electron microscopy revealed apoptotic changes of the liver cells in 20 mg/kg group.

CONCLUSIONThe slow accumulation of trace chromium (VI) after metal-on-metal hip arthroplasty may cause oxidative stress and changes in the oxidative stress system in the liver cells.

Animals ; Apoptosis ; Chromium ; administration & dosage ; toxicity ; Environmental Exposure ; Glutathione ; metabolism ; Hepatocytes ; metabolism ; pathology ; Malondialdehyde ; metabolism ; Mice ; Oxidative Stress ; Reactive Oxygen Species ; metabolism ; Superoxide Dismutase ; metabolism ; Toxicity Tests, Chronic

OBJECTIVEIn vitro model of hydrogen peroxide induced apoptosis of SW-480 cells was used to investigate the role of NF-kappaB in the pathogenesis of reactive oxygen species induced apoptosis of intestinal epithelial cells.

METHODSUltra-structural changes were observed. Apoptosis of SW-480 cell line was determined by Annexin-V and PI double-stained flow cytometry. Nuclear translocation of NF-kappaB was determined by anti-NF-kappaB polyclonal antibody and EB double-staining. NF-kappaB activity was studied by electrophoretic mobility shift assays. RT-PCR was performed to study expression of NF-kappaB mRNA.

RESULTSHydrogen peroxide led to apoptosis of SW-480 cells, condensed or semilunar chromatin even apoptotic bodies could be observed. Nuclear translocation of NF-kappaB, increase of NF-kappaB activity and expression of NF-kappaB mRNA were found simultaneously.

CONCLUSIONSEarly activation of NF-kappaB may be one of the mechanisms of apoptosis in intestinal epithelial cells by reactive oxygen species.

Apoptosis ; Humans ; Hydrogen Peroxide ; toxicity ; Intestinal Mucosa ; metabolism ; Microscopy, Confocal ; NF-kappa B ; metabolism ; Reactive Oxygen Species ; toxicity ; Tumor Cells, Cultured

This study investigated the conjoined cellular oxidative damage of human embryo kidney 293T (HEK293T) cells induced by cadmium chloride (CdCl(2)) and nanometer titanium dioxide (nano-TiO(2)). RT-PCR technique was used to detect the expressions of Heme oxygenase-1 (HO-1) and 8-oxoguanine DNA glycosylase (OGG1). The activities of superoxide dismutase (SOD) and catalase enzyme (CAT) and concentrations of reactive oxygen species (ROS) and maldondialdehyde (MDA) were measured by different approaches. The results showed that CdCl(2) and nano-TiO(2) at a low concentration of 0.75 total toxic unit (TU) exerted an additive effects on HO-1 gene expression, CAT activities and MDA concentrations. When the total TU was increased to 1 or 1.25 TU, the interaction was synergetic. Moreover, the mixture with high proportion of CdCl(2) produced an additive effect on the OGG1 gene expression, and the interaction was changed to be synergetic when the concentration of CdCl(2) was lower than or equal to that of nano-TiO(2). Synergetic effects of CdCl(2) and nano-TiO(2) on cellular oxidative damage of HEK293T cells were found as indicated by the changes in the SOD activities and ROS concentrations. It was concluded that CdCl(2) and nano-TiO(2) exerts synergistic effects on the cellular oxidative damage of HEK293T cells, and the sensitivity of these indicators of oxidative damage varies with the proportion of CdCl(2) and nano-TiO(2) in the mixture.
Cadmium Chloride ; toxicity ; Drug Synergism ; HEK293 Cells ; Humans ; Kidney ; cytology ; Nanoparticles ; Oxidative Stress ; drug effects ; Reactive Oxygen Species ; metabolism ; Superoxide Dismutase ; metabolism ; Titanium ; toxicity