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 identify the role of reactive oxygen species (ROS) formation on cell death induced by Ent-11alpha-hydroxy-15-oxo-kaur-16-en-19-oic-acid (5F) in HepG2 cells.

METHODMTT assay was used to determine the effect of 5F on proliferation of HepG2 cells, and apoptotic morphological changes were assessed using Hoechst/PI assay. To evaluate intracellular ROS levels, a GENMED kit was used. HepG2 cells were treated with 5F for 24 h or with 1 mmol x L(-1) GSH for 1 h prior to treatment with 5F for 24 h, then cytoplasmic mono- and oligonucleosomes were assessed with Cell Death Detection ELISA kit.

RESULTThe cytotoxicity of 5F on HepG2 cells was elevated with increasing 5F concentrations, as evidenced by the cell viability assay, and the apoptotic changes such as chromatin condensation were confirmed by Hoechst/PI staining. The decrease in ROS generation was observed in HepG2 cells following treatment with 5F. Cytoplasmic mono- and oligonucleosomes induced by 5F were not changed by decreasing basal level of ROS-mediated signaling with GSH. Further more, induction of ROS production by cisplatinum (CDDP) was canceled by treatment with 5F and 5F revealed a additive effect to cell killing by CDDP.

CONCLUSION5F can not only induce apoptosis through non-ROS-depandent pathway, and can abate oxidant stress.

Apoptosis ; drug effects ; Cell Death ; drug effects ; Diterpenes ; toxicity ; Drugs, Chinese Herbal ; toxicity ; Hep G2 Cells ; Humans ; Pteris ; chemistry ; Reactive Oxygen Species ; metabolism

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

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