AIMTo compare the TAOC of quercetin, rutin, vitamin C, vitamin E in vitro and examine the effect of quercetin on TAOC of rat plasma after intragastric administration.

METHODSFe3+ reducing ability assay, UV spectrum analysis and HPLC analysis were used to measure TAOC of plasma and the contents of quercetin and rutin after intragastric administration.

RESULTSThe TAOC of quercetin was stronger than that of rutin and roughly equal to vitamin C and vitamin E in vitro. After intragastric administration of quercetin (40 mg/kg bw), the TAOC and content of quercetin in rat plasma increased significantly. Vitamin C also increased plasma TAOC significantly, but rutin and vitamin E didn't after intragastric administration. However, there was no remarkable absorption peak of quercetin on HPLC chromatograms and on the other hand, the peak areas of two unknown peaks near quercetin peak were increased after intragastric administration of quercetin.

CONCLUSIONThe antioxidant capacity of quercetin was stronger than rutin and comparable to vitamin C both in vitro and in vivo. After absorption, quercetin is metabolized to its derivatives.

Animals ; Antioxidants ; pharmacology ; Ascorbic Acid ; pharmacology ; Male ; Quercetin ; pharmacology ; Rats ; Rats, Wistar ; Rutin ; pharmacology ; Vitamin E ; pharmacology

Apoptosis ; Ascorbic Acid/pharmacology* ; Brain Neoplasms ; Cell Line, Tumor ; Glioma ; Humans ; Temozolomide/pharmacology*

OBJECTIVETo investigate whether ascorbic acid could enhance the efficacy of arsenic trioxide (As(2)O(3)) combined with 2, 3-dimethoxy-1, 4-naphthoquinone (DMNQ) in inducing the apoptosis of leukemia cell line U937 and its possible mechanism.

METHODSFlow cytometry and electron microscopy were applied to detect apoptosis of U937 cells after treatment with various combinations of As(2)O(3), DMNQ and ascorbic acid for 24 hours.

RESULTSAs(2)O(3) and DMNQ induced-apoptosis of U937 cells was enhanced (35.24%-->61.20%) upon cotreatment with ascorbic acid. Catalase could reverse this effect of DMNQ. Ascorbic acid had no effect on DMNQ-induced apoptosis of U937 cells.

CONCLUSIONAscorbic acid enhanced the apoptosis of U937 cells via reactive oxygen species-dependent pathway in the presence of As(2)O(3).

Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Ascorbic Acid ; pharmacology ; Drug Synergism ; Flow Cytometry ; Humans ; Naphthoquinones ; pharmacology ; Oxides ; pharmacology ; U937 Cells

OBJECTIVETo explore arsenic-induced oxidative stress and the protective efficacy of α-lipoic acid and vitamin c.

METHODS50 male SD rats were randomly divided into 5 groups. Ten rats (the control group) were exposed to deionized water for 6 weeks, and the others were alone exposed to sodium arsenite (50 mg/L water) for 6 weeks, at the same time, three group rats were administered intragastrically (i.g.) with α-lipoic acid 10 mg×kg(-1)×d(-1) and vitamin C 25 mg×kg(-1)×d(-1) either alone or in combination. At the end of experiment, blood was drawn from abdominal aorta, and then the blood, brain and liver of rats were used for biochemical assays, including blood glutathione (GSH), δ-aminolevulinic acid dehydratase (δ-ALAD ), reactive oxygen species (ROS) and oxidized glutathione (GSSG) level. At the same time, the super oxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, catalase (CAT) activity, ATPase activity of brain and liver were determined. The caspase activity of brain were also determined.

RESULTSThere were a significant increase in ROS level (P < 0.05), but a significant decrease in δ-ALAD activity (P < 0.01) in the chronic arsenic toxicity model group compared with the control group. These alterations were marginally restored by co-administration of vitamin C and α-lipoic acid individually, while significant recovery was observed in the animals supplemented with both the antioxidants together with arsenite in rat (P < 0.05). At the same time, there was a significant increase in the ROS and TBARS level of the brain and liver (P < 0.05), and caspase activity of the brain (P < 0.05), while there was a significant decrease in antioxidant enzymes and ATPase activity on arsenite exposure in rats (P < 0.05). These alterations were also marginally restored by co-administration of vitamin C and α-lipoic acid individually, while significant recovery was observed in the animals supplemented with both the antioxidants together with arsenite in rat (P < 0.05).

CONCLUSIONSArsenite-induced oxidative stress can be significantly protected by co-administration of α-lipoic acid and vitamin C individually, but the best effects could be observed with combined administration of two antioxidants during arsenite exposure in animals. The dietary intervention of or supplementation with natural dietary nutrients is possible to prevent the effects of arsenic in populations of risk.

Animals ; Arsenic Poisoning ; metabolism ; Ascorbic Acid ; pharmacology ; Male ; Oxidative Stress ; drug effects ; Rats ; Rats, Sprague-Dawley ; Thioctic Acid ; pharmacology

OBJECTIVE: To study synergistic effect of Vitamin C (VitC) combined with arsenic trioxide (As2 O3)-on human laryngocarcinoma Hep-2 cell line apoptosis. METHOD: Human laryngocarcinoma cell line Hep-2 was cultured in vitro, and incubated with As2 O3 or jointly with VitC. The inhibition ability of Hep-2 cells was determined by methyl thiazolyl tetrazolium (MTT) assay, while the apoptosis was mensurated by the flow cytometry with Annexin-V/PI. RESULT: Compared with the use of As2 O3 separately, the combination of As2 O3 and VitC could increase the inhibition ability and the apoptosis rate of Hep-2 cells markedly (P < 0.05). CONCLUSION Combination of As2 O3 with VitC could markedly increase arsenic trioxide (As2 O3)-induced apoptosis of Hep-2 cells.
Apoptosis ; drug effects ; Arsenic Trioxide ; Arsenicals ; pharmacology ; Ascorbic Acid ; pharmacology ; Cell Line, Tumor ; Drug Synergism ; Humans ; Oxides ; pharmacology

Objective: To investigate the effects of cadmium (Cd) on antioxidant enzymes in testis of mice and the protective effect of vitamin C (VC). Methods: A total of 72 male Kunming mice of clean grade were divided into four groups (n=18): the control group, the Cd group (CdCl₂ 3 mg/kg), the VC group (200 mg/kg), and the VC (200 mg/kg) +Cd group (CdCl₂ 3 mg/kg). Mice were poisoned once a day, exposed for 1 and 3 days and were treated with VC at the same time. Twenty-four hours after exposure on the 1st and 3rd day, half of the mice in each group were weighed, the serum and testis tissues were collected. Testicular organ coefficient, malondialdehyde (MDA) and superoxide dismutase (SOD) in serum and testis tissues, and glutathione peroxidase (GSH-Px), reduced glutathione (GSH), oxidized glutathione (GSSG) and total glutathione (T-GSH) in testis tissues were detected. Results: Compared with the control group, the body weight and testicle organ coefficient of mice in the Cd group were decreased on the 1st and 3rd day; after 3 days of exposure, the serum SOD in the Cd group was decreased significantly and MDA was increased significantly (P＜0.05); the levels of SOD, GSH-Px, T-GSH and GSH/GSSG of testis in the Cd group were increased significantly on the 1st day (P＜0.05), while all the above indexes were decreased significantly on the 3rd day (P＜0.05), and the content of MDA was increased significantly on the 1st and 3rd days in the Cd group (P＜0.05); after VC treatment, the degree of reduction was decreased. Compared with the Cd group, the serum SOD and MDA levels in the VC+ Cd group were significantly different after 3 days of exposure (P＜0.05); the changes of SOD, GSH-Px, T-GSH and GSH/GSSG levels of the testis in the VC+ Cd group were significantly different on the 1st and 3rd day of exposure (P＜0.05), and the MDA level of the testis in the VC+ Cd group was decreased significantly on the 3rd day of exposure (P＜0.05). Compared with the Cd group for 1 day, the level of serum SOD exposed for 3 days was decreased significantly (P＜0.05), and the changes of testis indexes were also significantly different (P＜0.05). Conclusion: VC treatment can improve the antioxidant function of cadmium-loaded mice to some extent, and has protective effect on oxidative damage of testis.
Animals ; Antioxidants/pharmacology* ; Ascorbic Acid/pharmacology* ; Cadmium/toxicity* ; Glutathione ; Glutathione Disulfide/pharmacology* ; Glutathione Peroxidase ; Male ; Superoxide Dismutase ; Testis

OBJECTIVETo explore the effects and mechanisms of ascorbic acid (AA) and sodium selenite (SS) on growth inhibition and redifferentiation in human gastric cancer cells.

METHODSIn the present study, trypan blue dye exclusion method was used to determine the cell growth curve and mitotic index, cell electrophoresis and colonogenic potential were used as the indexes of redifferentiation. In order to find out the mechanisms of redifferentiation, the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT) were assayed, the content of malondialdehyde (MDA), reduced glutathione (GSH) and H2O2 were evaluated.

RESULTSAfter treatment with AA 3 mol/L + SS 2 mu mol/L, the growth rate and mitotic index of human gastric cancer cells (MGc-803) decreased remarkably. The indexes related with cell malignancy were alleviated. For example, cell surface charge was obviously decreased, the electrophoresis rate was dropped from 2.21 to 1.15 mu m.s-1.V-1.cm-1. The indexes related with cell redifferentiation were promoted. For example, the colonogenic potential was decreased to 93.5%. These results indicated that redifferentiation of human gastric cancer cells was successfully induced by AA + SS. The activities of SOD and GPX were significantly higher, while the activity of CAT was slower in treated group than that in the control. The content of MDA was slightly decreased, GSH was sharply decreased, and H2O2 content was dramatically increased.

CONCLUSIONThese results indicated that combination of ascorbic acid and sodium selenite may induce the redifferentiation of human gastric cancer cells and inhibit cell growth by virtue of enhancing the activities of antioxidative enzymes and inducing the formation of H2O2, and altering the cell redox status. Combination of ascorbic acid and sodium selenite may be a potent anticancer agent for human gastric cancer.

Antioxidants ; pharmacology ; Ascorbic Acid ; pharmacology ; Catalase ; pharmacology ; Cell Differentiation ; Glutathione Peroxidase ; pharmacology ; Humans ; Mitotic Index ; Sodium Selenite ; pharmacology ; Stomach Neoplasms ; pathology ; Superoxide Dismutase ; pharmacology ; Tumor Cells, Cultured

OBJECTIVESTo investigate the effects of newborn bull serum(NBS), vitamin C and vitamin E on cryopreservation of mouse seminiferous epithelial cells.

METHODSThe seminiferous epithelial cells from 7-day-old mice were cryopreserved in different freezing solutions. The cell recoveries were examined by Trypan blue exclusive staining after thawing. The freezing solutions composed of DMEM, 10% dimethylsulphoxide(DMSO), and 0, 5%, 10%, or 20% NBS, respectively, or composed of DMEM, 10% DMSO, 10% NBS, and 150 micrograms/ml vitamin C or 50 micrograms/ml vitamin E, respectively.

RESULTSThe cell recoveries in freezing solution containing 0, 5%, 10%, or 20% NBS were 83.4%, 84.7%, 85.7% and 83.6%, respectively. There were no significant differences between them. The cell recoveries in freezing solution containing vitamin C or vitamin E were 88.0% and 82.9%, respectively. There was no significant differences compared with that in freezing solution containing 10% DMSO and 10% NBS.

CONCLUSIONSNBS, vitamin C and vitamin E have no significant protecting effects on mouse seminiferous epithelial cells, and can not significantly improve the cell recoveries.

Animals ; Ascorbic Acid ; pharmacology ; Cattle ; Cryopreservation ; Epithelial Cells ; physiology ; Fetal Blood ; physiology ; Male ; Mice ; Seminiferous Epithelium ; cytology ; Vitamin K ; pharmacology

OBJECTIVETo explore the putative effects of Vitamin C (Vit C) on inhibition of human leucocyte antigen class I (HLA-I) expression of human peripheral blood mononuclear cells (HPBMCs) induced by deoxynivalenol (DON) in vitro.

METHODSThe effects of Vit C on the changes of HLA-I expression of HPBMCs induced by DON in vitro were evaluated with cell culture, flow cytometry (FCM), Western blotting and immunocytochemical methods.

RESULTSFCM analysis showed that HLA-I expression of HPBMCs in DON treated cells was significantly lower than that in controls (FI 0.88 +/- 0.02 vs 1.00 +/- 0.03, P < 0.05). As compared with DON group, the HLA-I expressions of HPBMCs in the two Vit C (25 micromol/L and 100 micromol/L) pretreatment groups were all significantly increased (1.15 +/- 0.06 and 1.10 +/- 0.02 vs 0.88 +/- 0.02, P < 0.05). Exposure to different dosage of Vit C alone could dramatically increase the expression of HLA-I of HPBMCs in vitro as compared with that in the normal control (FI for 25 micromol/L and 100 micromol/L Vit C treatment group was 1.28 +/- 0.03 and 1.25 +/- 0.05 respectively, P < 0.05). Immunocytochemical results showed that the percentages of HLA-I positive expression of HPBMCs in Vit C pretreatment groups at different dosages were significantly higher than those in DON group (70.10 +/- 6.90)%, (64.50 +/- 5.50)% vs (42.20 +/- 4.30)%, P < 0.05. Western blotting confirmed the results of FCM and immunocytochemistry.

CONCLUSIONSVitamin C pretreatment at different dosages could reverse at some extent the inhibitive effects of DON on HLA-I expression of HPBMCs.

Ascorbic Acid ; pharmacology ; Cells, Cultured ; Flow Cytometry ; Histocompatibility Antigens Class I ; metabolism ; Humans ; Monocytes ; drug effects ; metabolism ; Trichothecenes ; pharmacology

OBJECTIVETo explore the effects of Vitamin C (Vit C) on the apoptosis and proliferation inhibition of human peripheral blood mononuclear cells (HPBMCs) induced by deoxynivalenol (DON) in vitro.

METHODSThe effects of Vit C pretreatment at different dosages (25 micromol/L and 100 micromol/L) on apoptosis, apoptosis related genes expression and proliferation inhibition of HPBMCs induced by DON were evaluated with cell culture, flow cytometric DNA analysis and Western blotting.

RESULTSFlow cytometry (FCM) analysis showed that the apoptosis rate of HPBMCs in 2000 microg/L DON group was (28.82 +/- 1.67)%, which was significantly higher than that in control group (14.07 +/- 0.70, P < 0.05). Compared with DON group, the apoptosis rate of HPBMCs in 25 micromol/L Vit C pretreatment group was significantly decreased (28.82 +/- 1.67)% vs (22.39 +/- 1.05)%, P < 0.05, while that in 100 micromol/L Vit C pretreatment group was obviously increased (36.07 +/- 2.92)%, P < 0.05. Western blotting analysis showed that the expression of Bax and Caspase-3 up-regulated by DON was markedly decreased, while the expression of Bcl-2 down-regulated by DON was increased by 25 micromol/L Vit C pretreatment (P < 0.05). 100 micromol/L Vit C pretreatment could further increase the expression of Bax and Caspase-3 of HPBMCs induced by DON, while no significant effects on the Bcl-2 expression induced by DON were seen. FCM analysis showed that the proliferation index of HPBMCs in Vit C pretreatment groups at different dosages was all dramatically increased as compared with that in DON groups (P < 0.05).

CONCLUSION25 micromol/L Vit C pretreatment could at certain extent inhibit the apoptosis and reverse the abnormal expression of apoptosis related genes of HPBMCs induced by DON in vitro, while 100 micromol/L Vit C pretreatment could further increase the apoptosis rate of HPBMCs induced by DON. Vit C pretreatment could reverse the proliferation inhibition of HPBMCs induced by DON in vitro.

Apoptosis ; drug effects ; Ascorbic Acid ; pharmacology ; Cell Proliferation ; drug effects ; Cells, Cultured ; Humans ; Monocytes ; cytology ; drug effects ; Trichothecenes ; pharmacology