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

In an attempt to clarify the protective action of an antioxidant agent against acute toxicity of thioacetamide (TAA) and in order to throw some light on an satisfying concept of the mechanism of its action, a single dose of alphatocopherol (200 mg per kg) was given orally by stomch tube to male mice prior to the administration of thioacetamide in a dose of 200 mg per kg of body weight. Sections of liver samples, obtained from the mice which were sacrificed at intervals of 3, 6, 9, or 12 hours after TAA administration, were stained using the methyl green-pyronin technique. At 3 hours following TAA administration, the pretreatment with alpha-tocopherol inhibited almost completely such alterations of the hepatocytes in the animals given TAA alone, as revealed by loss and clumping of cytoplasmic pyroninophilic granules in the periportal zone of the lobule. At 6, 9, and l2 hours, the prevention of alpha-tocopherol was incomplete in degree and extent. The changes of the hepatocytes were more intense and extensive in the TAA-treated 6 to 12 hour-groups than in the 3 hour-group of TAA-treated ones. Some discussion is given of the mechanism of TAA toxicity, with respect to the microsoma1 lipid peroxidation.
Acetamides/poisoning* ; Animal ; Hepatitis, Toxic/pathology* ; Hepatitis, Toxic/prevention & control ; Liver/pathology* ; Male ; Mice ; Vitamin E/pharmacology* ; Vitamin E/therapeutic use

A novel oral delivery system that TPGS modified docetaxel proniosomes, DTX-TPGS-PN, was developed and the characterization after hydration was observed. Firstly, Doce-TPGS-PN was optimized by investing the factors, including the type of surfactant, methods of adding TPGS, content of TPGS and the molar ratio of span40/cholesterol, which may affecting the particle size, encapsulation efficiency and instantaneous release of drug in the formulation. Then, the morphology, particle size, Zeta potential, encapsulation efficiency and in vitro release of the formulation were evaluated. The result showed that hydrated nanoparticles of DTX-TPGS-PNs were (93 ± 6.5) nm in size,(-83.95 ± 3.69) mV in zeta potential, (97.31 ± 0.60)% in encapsulation efficiency, exhibiting spherical morphology and biphasic release process that a low burst effect within the first 0.5 hour and a relative-sustained release for the next several hours in PBS. These results indicate the oral delivery system of DTX-TPGS-PN was successfully built with good properties.
Chemistry, Pharmaceutical ; methods ; Particle Size ; Polyethylene Glycols ; chemistry ; Taxoids ; chemistry ; pharmacology ; Vitamin E ; analogs & derivatives ; chemistry

The Protective effect of vitamin E and selenium against peroxidative damage in white blood cells was studied. Forty-eight male rats (~100g BW) were divided into four groups and were fed with a torula yeast based diet deficient in Vit.E and Se. Vit.E (100IU/Kg diet) and Se (0.3ppm) supplementation increased the total peritoneal cell (P.C) population and cell survival rate. Selenium supplementation decreased the hydrogen peroxide generation (half of the control) significantly and Vit.E supplementation reduced the malonaldehyde production during phagocytosis in vitro. However, superoxide generation was not affected by the supplementation of Vit.E or Se. There were no significant differences in catalase activity between groups but glutathione peroxidase activity was increased about twofold by Se supplementation with no effect of Vit.E. In a separate experiment, activated alveolar macrophages were obtained from BCG infected rabbits fed a diet supplemented with Vit.E (100 IU/Kg diet) or Se (0.3 ppm). Se supplementation increased glutathione peroxidase in cells, and both Vit.E and Se increased the cell survival rate during phagocytosis as compared to the control. Both Vit.E and Se are necessary to protect host cells from peroxidative damage during phagocytosis.
Animal ; Macrophages/drug effects ; Macrophages/physiology* ; Male ; Peroxides/metabolism* ; Phagocytosis/drug effects* ; Rats ; Selenium/pharmacology* ; Vitamin E/pharmacology*

AIMTo evaluate the protective/ameliorative effects of vitamin E (vit E) on ethane dimethane sulfonate (EDS)-induced testicular toxicity in rats.

METHODSThe rats were assigned to eight groups, seven rats in each, and were injected intraperitoneally with vehicle, a single dose of ethane dimethane sulfonate (EDS) (75 mg/kg bodyweight), vit E (100 mg/kg bodyweight) or EDS + vit E for 3? days. Thereafter, the rats were weighed, anaesthetized with ether and killed by cervical dislocation. The left testis weights were recorded and the relative testis weights were calculated. The left testes were processed for routine paraffin embedding. Three right testes from each group were taken randomly and then processed for routine electron microscopy. Tissue sections were examined using light and electron microscopy, and were scored for histopathological changes.

RESULTSVit E coadministration did not prevent the bodyweight loss on days 3 and 7. However, vit E administration prevented the EDS-induced testicular-weight loss in rats that received vit E for 3 days but not 7 days. The relative testis weight was higher on day 3 (instead of on day 7) than other groups. Nevertheless, the testis histology was not markedly protected by vit E in the EDS-treated rats. Detailed microscopic assessment showed few Leydig cells and abundant fibroblast-like cells indicating only some protection.

CONCLUSIONVit E cotreatment showed partial protective effects on the testicular weight and testicular histology in rats that received EDS.

Animals ; Antitoxins ; pharmacology ; Male ; Mesylates ; toxicity ; Rats ; Rats, Sprague-Dawley ; Testis ; drug effects ; pathology ; Vitamin E ; pharmacology

The inhibitory effect of selenium, vitamin E, and BHA on DMBA-induced mammary tumorigenesis in rats was investigated. Dietary vitamin E (200 IU/Kg diet) alone could not reduce the tumor incidence at 25 weeks after DMBA administration (10mg DMBA/rat) when selenium was deficient. Selenium supplementation (2ppm in drinking water) to rats fed a practical diet (0.17 ppm Se) reduced the tumor incidence to 14.3% from 75% at 27 weeks after DMBA administration. Dietary supplementation of BHA (0.75%) also reduced the incidence of DMBA-induced mammary tumor to 42.9% at 27 weeks after DMBA-treatment. Rats fed a diet deficient in both selenium and vitamin E contained significantly lower glutathione peroxidase activity and higher malondialdehyde in muscle. However, supplementation of selenium or BHA to the rats fed a practical diet did not alter the malondialdehyde content and glutathione peroxidase activities in muscle, skin and mammary gland. Dietary selenium increased the tissue selenium level. DMBA-induced mammary tumorigenesis was reduced by antioxidants tested but the anticarcinogenic effect of selenium or BHA seems to be independent of glutathione peroxi-dase activity.
9,10-Dimethyl-1,2-benzanthracene ; Animal ; Antioxidants/pharmacology* ; Butylated Hydroxyanisole/pharmacology ; Female ; Mammary Neoplasms, Experimental/pathology* ; Rats ; Selenium/pharmacology ; Vitamin E/pharmacology

Administration, Oral ; Adult ; Antioxidants ; administration & dosage ; pharmacology ; Ascorbic Acid ; administration & dosage ; pharmacology ; Humans ; Lipid Peroxidation ; drug effects ; Male ; Middle Aged ; Occupational Health ; Vitamin E ; administration & dosage ; pharmacology

Increased generation of ROS causes the lipid oxidation of the membrane of spermatozoa, but antioxidant vitamins play an important role in reproduction and help clear away ROS and protect the sperm membrane from lipid oxidation. This review focused on the effect of antioxidant vitamins on male reproduction and in the treatment of male infertility.
Animals ; Antioxidants ; pharmacology ; therapeutic use ; Ascorbic Acid ; pharmacology ; therapeutic use ; Humans ; Infertility, Male ; drug therapy ; Lipid Peroxidation ; drug effects ; Male ; Reactive Oxygen Species ; adverse effects ; Reproduction ; drug effects ; Vitamin A ; pharmacology ; therapeutic use ; Vitamin E ; pharmacology ; therapeutic use

OBJECTIVETo observe the protective effects of vitamin E on the testicular injury by cyclophosphamide in mice, and the correlative mechanism.

METHODSFifty sexually mature male mice were randomly divided into five groups: the cyclophosphamide group (the CP group), the low-dose vitamin E group (the low-dose group), the middle-dose vitamin E group (the middle-dose group), the high-dose vitamin E group (the high-dose group), the matched control group (the control group). The first four groups were given cyclophosphamide by gavage at a dose of 5 mg/(kg x d). The low-dose group, the middle-dose group and the high-dose group were given vitamin E by subcutaneous injection at doses of 30 mg/(kg x d), 50 mg/(kg x d) , 70 mg/(kg x d) after 4 h of cyclophosphamide treatment. The control group was gavaged with equivalent normal saline. The treatment period for all groups was 28 days. The level of plasma FSH, LH, T and the activity of testicular SOD, GSHPx, CAT and the level of testicular MDA were detected. The histological structure and the ultrastructure of the testis were examined by light microscope and electron microscope.

RESULTSAs compared with the CP group, the plasma FSH, LH, T level and the SOD, GSHPx, CAT activity in the middle-dose group and the high-dose group were higher (P< 0.05, P< 0.01), MDA level significantly lower(P<0.01). The histological structure and the ultrastructure of the testis were in the normal range.

CONCLUSIONVitamin E has protective effects on the testicular injury by cyclophosphamide in mice. The possible mechanism of vitamin E may be its scavenging free radical and antioxidant effects, as well as it may have some stimulatory effects on gonadotrophin releasing of pituitary anterior lobe.

Animals ; Antioxidants ; pharmacology ; Cyclophosphamide ; antagonists & inhibitors ; toxicity ; Dose-Response Relationship, Drug ; Male ; Mice ; Mice, Inbred Strains ; Random Allocation ; Testis ; drug effects ; pathology ; Vitamin E ; pharmacology

AIMTo investigate the effect of formaldehyde (FA) on testes and the protective effect of vitamin E (VE) against oxidative damage by FA in the testes of adult rats.

METHODSThirty rats were randomly divided into three groups: (1) control; (2) FA treatment group (FAt); and (3) FAt + VE group. FAt and FAt + VE groups were exposed to FA by inhalation at a concentration of 10 mg/m(3) for 2 weeks. In addition, FAt + VE group were orally administered VE during the 2-week FA treatment. After the treatment, the histopathological and biochemical changes in testes, as well as the quantity and quality of sperm, were observed.

RESULTSThe testicular weight, the quantity and quality of sperm, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione (GSH) were significantly decreased whereas the level of malondialdehyde (MDA) was significantly increased in testes of rats in FAt group compared with those in the control group. VE treatment restored these parameters in FAt + VE group. In addition, microscopy with hematoxylin-eosin (HE) staining showed that seminiferous tubules atrophied, seminiferous epithelial cells disintegrated and shed in rats in FAt group and VE treatment significantly improved the testicular structure in FAt + VE group.

CONCLUSIONFA destroys the testicular structure and function in adult rats by inducing oxidative stress, and this damage could be partially reversed by VE.

Animals ; Antioxidants ; pharmacology ; Epididymis ; drug effects ; pathology ; Formaldehyde ; toxicity ; Male ; Oxidative Stress ; drug effects ; physiology ; Rats ; Rats, Sprague-Dawley ; Sperm Count ; Testis ; drug effects ; pathology ; Vitamin E ; pharmacology