BACKGROUND: Coenzyme Q10 is an endogenous lipid soluble antioxidant that scavenges reactive oxygen species (ROS) directly, inhibits biomolecule oxidation, and affects antioxidant defense in vivo. Kinetin (N6-furfuryladenine) belongs to the family of N6-substituted adenine derivatives known as cytokinins. Kinetin also exerts anti-aging effects. Commercial products of coenzyme Q10 and kinetin are developed and are selling as a rejuvenating drug. However, the action mechanisms of kinetin are not fully known, though it has been suggested to act both as an inhibitor of reactive oxygen species (ROS) formation and as a scavenger of ROS. Thioctic acid (alpha-Lipoic acid), which becomes a powerful antioxidant in its reduced form, has been suggested as a dietary supplement to treat diseases associated with excessive oxidant stress. Exposure of the skin to ultraviolet (UV) radiation, particulary UVB (290-320nm), causes adverse biological effects, including alterations in cutaneous immune cells, photoaging and photocarcinogenesis. Several studies have shown that coenzyme Q10, kinetin, and thioctic acid afforded the protection effects against UVB-induced inflammatory responses and photoaging. Objective and Method: In this study, we investigated the effects of coenzyme Q10, kinetin and thioctic acid on UVB irradiated human skin fibroblasts using a viability test, thiobarbituric acid assay and Northern blot analysis. RESULT: Cell survival curves after UVB irradiation showed a dose dependent decremental pattern by trypan blue exclusion assay. Only 30% of dermal fibroblasts survived at 150mJ/cm2 UVB irradiation. The damage was associated with cell membrane lipid peroxidation, as shown by accumulation malondialdehyde (MDA). By pre-cultivation with coenzyme Q10, kinetin and thioctic acid, a significant protection effect was noted as an increase in the absolute number of surviving cells and marked decrease in the levels of MDA. CONCLUSION: Coenzyme Q10, kinetin, and thioctic acid, which have been newly accepted as having UV protection properties, are effective membrane peroxidation inhibitors and inhibitors of reactive oxygen species (ROS) formation and scavenger of ROS.
Humans ; Oxidants

It has been being some studies on biomedical effects of mulberry leaves in the world. Mulberry trees are widly cultivated in VietNam to take leaves for fed of silkworm. However, there were few studies on extraction, determination and antioxidation of mulberry leaves in VietNam. Objectives: extraction and determination of polyphenol from mulberry leaves. Evaluation of antioxidant capacities of mulberry leaf extract powders. Methods: Mulberry leaf extract powder were extracted from mulberry leaves by five solvens: methanol 100%, methanol 75%, n-hexan 100%, ethylacetat 100%. Polyphenol concentration of the extracts are determined by ferrous sulphate and follin reagent assay. Antioxidant capacities of the powders are based on peroxidation of linoleic acid at 40oC. Results: Among five solvens, the extract by methanol 75% from 50g dried leaves is best. The powder is 1.94g with 2.62% of polyphenol. Polyphenol concentraion of the extract powders are determined by two methods: ferrous sulphate and follin reagent. The result with ferrous sulphate method is more accurate than follin reagent method. The mulberry leave extract powders inhibited linoleic acid peroxidation at the 1h and 12h of reaction (only 15.5% to 42.2% linoleic acid peroxidated) in comparison with control (100% linoleic acid peroxidated). Conclusions: Polyphenol from mulberry leaves was extracted by some solvens. Among them extraction of polyphenol by methanol 75% is best. Polyphenol concentration of extract powders can be dedermined by ferrous sulphat. The extract powders from mulberry leaves exhibited antioxidant capacities in vitro. The extract powder by methanol 75% showed highest antioxidant capacitiy.
Oxidants ; Morus

PURPOSE: The modification of radiation-induced apoptosis by EGCG, known as antioxidants or oxidants, was studied in mice spleens irradiated with a lethal dose. MATERIALS AND METHODS: Male C57BL/6 mice were divided into control, irradiation-only, and EGCG (100 mg/kg i.p. 1 h before irradiation) pretreatment groups. The mice were irradiated with a single whole-body dose of 7 Gy. The apoptosis in the spleens after irradiation of the lethal dose were analyzed by TUNEL assay. In addition, the expression levels of the Bax and Bcl-2 proteins were quantified using a Western blotting method. RESULTS: The induction of apoptosis was detected in the splenic white pulp. The highest level of apoptosis was detected at 8 hours after irradiation. No significant difference was identified by the apoptotic index (53.9% vs. 52.1%, p=0.328) and relative Bax protein expression (0.86 vs. 0.81, p=0.335), between the irradiation-only and EGCG pretreatment group, respectively. However, a lower Bax/Bcl-2 ratio (1.64 vs. 0.97, p=0.037) and higher relative expression level of Bcl-2 protein (0.57 vs. 0.82, p=0.037) was measured in the EGCG pretreatment group. CONCLUSION: The EGCG pretreatment neither decreased the radiation-induced apoptosis in mice splenocytes, nor induced additional apoptosis.
Male ; Humans ; Oxidants

The diabetic patients are usually suffered from oxidation stress. Green tea is one of the good herbal medicines has been used for treatment of some diseases. Objectives: Evaluate change of antioxidant status in blood and effect of the green tea polyphenol on this change in the experimental diabetic rats. Methods: Using in vivo model to investigate some biological indicators in STZ - induced diabetic rats fed with high fat diet and to evaluate effect of the green tea polyphenol on the changes of these indicators. Results: Erythrocyte GPx activity and serum MDA concentration in STZ - induced diabetic rats was higher than that of normal and lipid metabolism disorder groups (p < 0.001) and effected of the green tea polyphenol. However, no change in erythrocyte SOD activity and plasma TAS level was observed. Conclusions: Green tea polyphenol improved blood antioxidant status in STZ - induced diabetic rats.
Diabetes Mellitus ; Tea ; Camellia sinensis ; Blood ; Oxidants

Background and Objectives. Neuroprotection agents may help improve the outcomes of large vessel ischemic stroke. This study aims to explore the role of Virgin Coconut Oil (VCO), with its well-documented anti-oxidant properties, in neuroprotection after transient occlusion of the extracranial internal carotid artery in a rat model of stroke. Methods. Twenty-three Sprague-Dawley rats were randomized into two groups: 1) control group (n=11) given distilled water, and 2) treatment group (n=12) given virgin coconut oil at 5.15 ml/kg body weight for seven days. Subsequently, the rats underwent transient right extracranial internal carotid artery occlusion (EICAO) for 5 minutes using non-traumatic aneurysm clips. At 4 and 24 hours after EICAO, the animals were examined for neurologic deficits by an observer blinded to treatment groups, then sacrificed. Eight brain specimens (4 from each group) were subjected to histopathologic examination (H & E staining) while the rest of the specimens were processed using triphenyltetrazolium chloride (TTC) staining to determine infarct size and area of hemispheric edema. Results. VCO treatment significantly improved the severity of neurologic deficit (1.42 ± 2.31) compared to the control distilled water group (4.09 ± 2.59) 24 hours after EICAO. Whereas, infarct size and percent hemispheric edema did not significantly differ between the two groups. Conclusion. Prophylactic treatment of VCO is protective against EICAO-induced neurologic deficits in a rat model. VCO shows great potential as a neuroprotective agent for large vessel ischemic stroke. However, more studies are necessary to elucidate the neuroprotective mechanisms of VCO therapy in ischemic stroke.
Coconut Oil ; Oxidants ; Antioxidants ; Neuroprotection ; Ischemia ; Stroke

In-depth knowledge of disinfection and sterilization is a key component of infection control. Sterilization completely removes a spore, whereas disinfection cannot. Disinfectants are classified as oxidants and non-oxidants. The decision regarding which method to apply is based on Spaulding's classification. In this article, disinfection and sterilization are thoroughly reviewed, and extensive information from basic to practical points is discussed.
Classification ; Disinfectants ; Disinfection* ; Infection Control ; Methods ; Oxidants ; Spores ; Sterilization*

In-depth knowledge of disinfection and sterilization is a key component of infection control. Sterilization completely removes a spore, whereas disinfection cannot. Disinfectants are classified as oxidants and non-oxidants. The decision regarding which method to apply is based on Spaulding's classification. In this article, disinfection and sterilization are thoroughly reviewed, and extensive information from basic to practical points is discussed.
Classification ; Disinfectants ; Disinfection* ; Infection Control ; Methods ; Oxidants ; Spores ; Sterilization*

The physiological activity of osteoblasts is known to be closely related to increased intracellular Ca2+ activity ([Ca2+]i) in osteoblasts. The cellular regulation of [Ca2+]i in osteoblasts is mediated by Ca2+ movements associated with Ca2+ release from intracellular Ca2+ stores, and transmembrane Ca2+ influx via Na+-Ca2+ exchanger, and Ca2+ ATPase. Reactive oxygen species, such as H2O2, play an important role in the regulation of cellular functions, and act as signaling molecules or toxins in cells. In this study, we investigated the effects of H2O2 on cellular Ca2+ regulation in osteoblasts by measuring intracellular Ca2+ activities using cellular calcium imaging techniques. Osteoblasts were isolated from the femurs and tibias of neonatal rats, and cultured for 7 days. The cultured osteoblasts were loaded with a Ca2+-sensitive fluorescent dye, Fura-2, and fluorescence images were monitored using a cooled CCD camera, and subsequently analyzed using image analyzing software. The results obtained are as follows: (1) The osteoblasts with lower basal Ca2+ activities yielded a transient Ca2+ increase, a Ca2+ spike, while osteoblasts with higher basal Ca2+ activities showed a continuous increase in [Ca2+]i leading to cell death. (2) Ca2+ spikes, generated after removing Na+ from superfusing solutions, were blocked by H2O2 and this was followed by a sustained increase in Ca2+ activity. (3) ATP- induced Ca2+ spikes were inhibited by pretreating with H2O2 and this was followed by a continuous increase of [Ca2+]i. When cells were pretreated with the exogenous nitric oxide (NO) donor S-Nitroso-N-acetylpenicilance (SNAP, 50 microM), treatments of ATP (1 mM) induced a Ca2+ spike-like increase, but [Ca2+]i did not return to the basal level. (4) The expression of inositol- 1,4,5-triphosphate receptor (IP3R) was enhanced by H2O2. Our results suggest that H2O2 modulates intracellular Ca2+ activity in osteoblasts by increasing Ca2+ release from the intracellular Ca2+ stores.
Animal ; Calcium/*metabolism ; Cells, Cultured ; Hydrogen Peroxide/*pharmacology ; Osteoblasts/*drug effects/*metabolism ; Oxidants/*pharmacology ; Rats

PURPOSE: Thioredoxin is an endogenous antioxidant which directly scavenges reactive oxygen species(ROS) and regenerates oxidatively damaged protein by reducing potential at the redox active disulfide(-Cys-Gly-Pro-Cys-) site. Under oxidative stress, thiredoxin plays a protective and adaptative role by inducing expressions. The aim of this study was to clarify the role of thioredoxin on oxidative neuronal cell injury. We investigated the protective effects of E. coli thioredoxin, also acting as a substrate for mammalian thioredoxin reductase, against oxidative neuronal cell injury under oxidative stresses such as hydrogen peroxide and diamide. METHODS: PC 12 cells were cultured in RPMI 1640 media containing 10% fetal calf serum and subcultured in 96-well plates. Each well contained 30,000 cells. Cells were treated with hydrogen peroxide or diamide 30 minutes after thioredoxin treatment and then incubated for 24 hours. Cytotoxicity and cellular viability were assessed by measuring of lactate dehydrogenase(LDH) release and MTT reduction. RESULTS: Thioredoxin not only decreased the cytotoxicity of PC 12 cell treated with hydrogen peroxide by decreasing LDH release and preventing the decrease of MTT reduction but also thioredoxin showed greater protective effects when simultaneously treated with hydrogen peroxide. Also, thioredoxin decreased cytotoxicity by decreasing LDH release from PC 12 cells damaged by diamide. Thioredoxin did not prevent the decrease of MTT reduction on PC 12 cells damaged by diamide. CONCLUSION: Thioredoxin protected PC 12 cells under oxidative stresses by directly scavenging and inhibiting oxidants such as hydrogen peroxide and diamide.
Diamide ; Hydrogen Peroxide ; Lactic Acid ; Neurons* ; Oxidants ; Oxidation-Reduction ; Oxidative Stress ; Oxygen ; Thioredoxin-Disulfide Reductase ; Thioredoxins*

BACKGROUND: Eckol purified from Ecklonia cava, a brown alga has been known to have cytoprotective effects on some cell lines against oxidants and ionizing radiation. However, there is no study about the effects of eckol on immune cells. METHODS: Bone marrow (BM)-derived dendritic cells (DCs) were used to demonstrate the immunomodulatory effects of eckol on DCs, such as viability, the expression of surface markers, allogeneic stimulating capacity using MTT, flow cytometric, (3)H-thymidine incorporation assay. RESULTS: Eckol did protect DCs against cytokine withdrawal-induced apoptosis in a concentration dependent manner based on MTT assay. And also, it increased the expression of MHC class II and CD86 (B7.2) molecules, maturation markers, on the surface of viable DCs gated in FACS analysis. Furthermore, eckol-treated DCs stimulated the proliferation of allogeneic CD4+ T lymphocytes compared to imDCs in (3)H-thymidine incorporation assay. CD4+ T lymphocytes activated with eckol-treated DCs produced the larger amount of IFN-gamma and IL-4 than those cells with imDCs. CONCLUSION: Taken together, we demonstrate in this study that eckol, a pure compound of Ecklonia cava, may modulate the immune responses through the phenotypic and functional changes of DCs.
Apoptosis ; Bone Marrow ; Cell Line ; Dendritic Cells* ; Interleukin-4 ; Oxidants ; Radiation, Ionizing ; T-Lymphocytes