Co-Administration of Vitamin E and Testosterone Attenuates The Atrazine-Induced Toxic Effects on Sperm Quality and Testes in Rats.

Rezaie Agdam H, Razi M, Amniattalab A, Malekinejad H, Molavi M.

Cell J. 2017 Jul-Sep;19(2):292-305. doi: 10.22074/cellj.2016.490. Epub 2017 Feb 22.

Abstract

OBJECTIVE:

Atrazine (ATZ) as a widely used herbicide is considered as a potent endocrine disrupter which adversely affects reproductive systems in both genders. This study aimed to assess the effects of testosterone (T)- and vitamin E (VitE)- alone and their coadministration on testicular function and sperm parameters after exposure to ATZ in rats.

MATERIALS AND METHODS:

In this experimental study, the rats (n=30) are assigned into the following 5 groups: control-sham group (n=6) receiving corn oil, ATZ group (n=6) receiving 200 mg/kg ATZ alone, ATZ+VitE group (n=6) receiving 150 mg/kg ATZ+VitE, ATZ+T group (n=6) receiving 400 µg/kg ATZ+T, and ATZ+VitE+T group (n=6) receiving ATZ+VitE+T for 48 consecutive days. Total antioxidant capacity (TAC), total thiol molecules (TTM), and malondialdehyde (MDA) were analyzed. Serum levels of T, luteinizing hormone (LH), and inhibin-B (IN-B) were also determined. Histological examination and sperm analysis were performed. The data were analyzed using Graph-Pad Prism software version 2.01.

RESULTS:

Co-administration of VitE and T significantly (P<0.05) increased ATZ-decreased TAC and TTM levels and reduced ATZ-increased MDA content. T and VitE significantly (P<0.05) increased serum levels of ATZ-reduced T (1.94 ± 0.96), IN-B (122.10 ± 24.33) and LH (0.40 ± 0.10). The T+VitE animals showed a reduction in apoptotic cells and an increase in Leydig cells steroidogenesis. Co-administration of T and VitE significantly (P<0.05) reduced the ATZ-induced DNA disintegrity and chromatin de-condensation. VitE and T protected germinal cells RNA and protein contents against ATZ-induced damages.

CONCLUSION:

T and VitE in simultaneous form of administration were able to normalize the ATZ-induced derangements through promoting antioxidant capacity and endocrine function.

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Chemical components, antioxidant potential and hepatoprotective effects of Artemisia campestris essential oil against deltamethrin-induced genotoxicity and oxidative damage in rats.

Saoudi M, Ncir M, Ben Ali M, Grati M, Jamoussi K, Allouche N, El Feki A.

Gen Physiol Biophys. 2017 Jul;36(3):331-342. doi: 10.4149/gpb_2016057.

Abstract

In the present study, we evaluated the antioxidant potential of Artemisia campestris essential oil (ACEO) and the possible protective effects against deltamethrin induced hepatic toxic effects. The ACEO showed radical scavenging activity with IC50 = 47.66 ± 2.51 µg/ml, ferric reducing antioxidant power (FRAP) potential (EC50 = 5.36 ± 0.77 µg/ml), superoxide scavenging activity (IC50 = 0.175 ± 0.007 µg/ml) and ˙OH scavenging activity (IC50 = 0.034 ± 0.007 µg/ml). The obtained results of phenolic profile demonstrated that phenolic compounds are the major contributor to the antioxidant activity of ACEO. GC-MS analysis revealed the presence of 61 components in which monoterpene hydrocarbons constitute the major fraction (38.85%). In in vivo study, deltamethrin exposure caused an increase of serum AST, ALT and ALP activities, hepatic malondialdehyde (MDA) (measured as TBARS) and conjugated dienes markers of lipid peroxidation (LPO), while antioxidant enzyme activities (SOD, CAT and GPx) decreased significantly. Furthermore, it induces DNA damage as indicated by DNA fragmentation accompanied with severe histological changes in the liver tissues. The treatment with vitamin E or ACEO significantly improved the hepatic toxicity induced by deltamethrin. It can be concluded that vitamin E and ACEO are able to improve the hepatic oxidative damage induced by deltamethrin. Therefore, ACEO is an important product in reducing the toxic effects of deltamethrin.

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Enhancement of apoptotic activities on brain cancer cells via the combination of γ-tocotrienol and jerantinine A.

Abubakar IB, Lim KH, Kam TS, Loh HS.

Phytomedicine. 2017 Jul 1;30:74-84. doi: 10.1016/j.phymed.2017.03.004. Epub 2017 Mar 10.

Abstract

BACKGROUND:

γ-Tocotrienol, a vitamin E isomer possesses pronounced in vitro anticancer activities. However, the in vivo potency has been limited by hardly achievable therapeutic levels owing to inefficient high-dose oral delivery which leads to subsequent metabolic degradation. Jerantinine A, an Aspidosperma alkaloid, originally isolated from Tabernaemontana corymbosa, has proved to possess interesting anticancer activities. However, jerantinine A also induces toxicity to non-cancerous cells.

PURPOSE:

We adopted a combinatorial approach with the joint application of γ-tocotrienol and jerantinine A at lower concentrations in order to minimize toxicity towards non-cancerous cells while improving the potency on brain cancer cells.

METHODS:

The antiproliferative potency of individual γ-tocotrienol and jerantinine A as well as combined in low-concentration was firstly evaluated on U87MG cancer and MRC5 normal cells. Morphological changes, DNA damage patterns, cell cycle arrests and the effects of individual and combined low-concentration compounds on microtubules were then investigated. Finally, the potential roles of caspase enzymes and apoptosis-related proteins in mediating the apoptotic mechanisms were investigated using apoptosis antibody array, ELISA and Western blotting analysis.

RESULTS:

Combinatorial study between γ-tocotrienol at a concentration range (0-24µg/ml) and fixed IC20 concentration of jerantinine A (0.16µg/ml) induced a potent antiproliferative effect on U87MG cells and led to a reduction on the new half maximal inhibitory concentration of γ-tocotrienol (i.e.tIC50=1.29µg/ml) as compared to that of individual γ-tocotrienol (i.e. IC50=3.17µg/ml). A reduction on undesirable toxicity to MRC5 normal cells was also observed. G0/G1 cell cycle arrest was evident on U87MG cells receiving IC50 of individual γ-tocotrienol and combined low-concentration compounds (1.29µg/ml γ-tocotrienol + 0.16µg/ml jerantinine A), whereas, a profound G2/M arrest was evident on cells treated with IC50 of individual jerantinine A. Additionally, individual jerantinine A and combined compounds (except individual γ-tocotrienol) caused a disruption of microtubule networks triggering Fas- and p53-induced apoptosis mediated via the death receptor and mitochondrial pathways.

CONCLUSIONS:

These findings demonstrated that the combined use of lower concentrations of γ-tocotrienol and jerantinine A induced potent cytotoxic effects on U87MG cancer cells resulting in a reduction on the required individual concentrations and thereby minimizing toxicity of jerantinine A towards non-cancerous MRC5 cells as well as probably overcoming the high-dose limiting application of γ-tocotrienol. The multi-targeted mechanisms of action of the combination approach have shown a therapeutic potential against brain cancer in vitro and therefore, further in vivo investigations using a suitable animal model should be the way forward.

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Effect of vitamin E on oxidative stress level in blood, synovial fluid, and synovial tissue in severe knee osteoarthritis: a randomized controlled study.

Tantavisut S, Tanavalee A, Honsawek S, Suantawee T, Ngarmukos S, Adisakwatana S, Callaghan JJ.

BMC Musculoskelet Disord. 2017 Jun 29;18(1):281. doi: 10.1186/s12891-017-1637-7.

Abstract

BACKGROUND:

This study was performed to evaluate the antioxidative and anti-inflammatory effects of vitamin E on oxidative stress in the plasma, synovial fluid, and synovial tissue of patients with knee osteoarthritis.

METHODS:

Seventy-two patients with late-stage knee osteoarthritis scheduled for total knee arthroplasty were randomized to take oral placebo (Group A) or 400 IU of vitamin E (Group B) once a day for 2 months before undergoing surgery. The blood levels of endpoints indicating oxidative stress or antioxidant capacity, Knee Society Score (KSS), Western Ontario and McMaster Universities Osteoarthritis Index score (WOMAC), and adverse effects were compared before and after the intervention between the two groups. At surgery, these redox endpoints and histological findings were compared between the synovial fluid and synovial tissue.

RESULTS:

In blood samples, the pre-intervention of oxidative stress and antioxidative capacity were not different between Group A and Group B. In post-intervention blood samples, the Malondialdehyde (Group A 1.34 ± 0.10, Group B 1.00 ± 0.09, p < 0.02), Alpha tocopherol(Group A 15.92 ± 1.08, Group B 24.65 ± 1.47, p < 0.01) and Trolox equivalent antioxidant capacity (Group A 4.22 ± 0.10, Group B 5.04 ± 0.10, 0 < 0.01) were significantly different between Group A and Group B. In synovial fluid samples, the Malondialdehyde (Group A 1.42 ± 0.12, Group B 1.06 ± 1.08, p 0.01), Alphatocopherol (Group A 4.51, Group B 7.03, p < 0.01), Trolox equivalent antioxidant capacity (Group A, 1.89 ± 0.06, Group B 2.19 ± 0.10) were significantly different between Group A and Group B. The pre-intervention WOMAC score and KSS score were not different between Group A and Group B. The post-intervention WOMAC score was significantly improved in all categories in Group B (Pain: Group A 27.26 ± 0.89, Group B 19.19 ± 1.43, p < 0.01; Stiffness: Group A 8.23 ± 0.79, Group B 5.45 ± 0.73, p 0.01; Function: Group A 94.77 ± 4.22, Group B 72.74 ± 6.55, p < 0.01). The post-intervention KSS score was significantly improved in all categories in Group B (Clinical: Group A 25.31 ± 14.33, Group B 33.52 ± 16.96, p < 0.01; Functional: Group A 41.43 ± 16.11, Group B 51.61 ± 19.60, p 0.02). Significantly fewer synovial tissue cells were stained with nitrotyrosine and hematoxylin-eosin in Group B than in Group A. There were no differences in adverse effects or surgical complications between the groups.

CONCLUSION:

Vitamin E is an effective antioxidant that can improve clinical symptoms and reduce oxidative stress conditions in patients with late-stage knee osteoarthritis.

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Ovarian Damages Produced by Aerosolized Fine Particulate Matter (PM2.5) Pollution in Mice: Possible Protective Medications and Mechanisms.

Gai HF, An JX, Qian XY, Wei YJ, Williams JP, Gao GL.

Chin Med J (Engl). 2017 Jun 20;130(12):1400-1410. doi: 10.4103/0366-6999.207472.

Abstract

BACKGROUND:

Ambient aerosol fine particulate matter (PM2.5) is associated with male reproductive toxicity in experiments and may have adverse effects in the female. However, studies evaluating the protective effects and precise mechanisms of aspirin, Vitamin C, Vitamin E, or ozone against toxic effects of PM2.5are sparse. This study was conducted to investigate the possible protective effects and mechanisms of aspirin, Vitamin C, Vitamin E, or ozone on fertility in female mice treated with PM2.5.

METHODS:

Eighty-four ICR mice were divided into six groups: control group, PM2.5group, PM2.5 + aspirin group, PM2.5 + Vitamin C group, PM2.5 + Vitamin E group, and PM2.5 + ozone group. PM2.5was given by intratracheal instillation every 2 days for 3 weeks. Aspirin, Vitamin C, and Vitamin E were given once a day by oral gavage for 3 weeks, and ozone was administered by intraperitoneal injection once a day for 3 weeks. The levels of anti-Müllerian hormone (AMH), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) were measured using enzyme-linked immunosorbent assay. Western blotting analysis was used to analyze the expressions of Bcl-2, Bax, and caspase-3 in ovaries. Changes in histological structure were examined by light microscope and electron microscopy was used to detect ultramicrostructure.

RESULTS:

The results demonstrated that PM2.5 decreased AMH levels (P < 0.001); however, aspirin (P < 0.001), Vitamin C (P < 0.001), Vitamin E (P = 0.001), and ozone (P = 0.002) alleviated the decrease. Changes of IL-6, TNF-α, 8-OHdG, Bax/Bcl-2, and caspase-3 in PM2.5group were increased compared to control group (P < 0.001), while in PM2.5 + aspirin, PM2.5 + Vitamin C, PM2.5 + Vitamin E, and PM2.5 + ozone groups, they were statistically decreased compared to PM2.5group (P < 0.001 or P< 0.05).

CONCLUSIONS:

PM2.5cause the damage of ovaries, and aspirin, Vitamin C, Vitamin E, and ozone antagonizes the damage. The protective mechanism is probably due to its ability to blunt the inflammatory and oxidative stress caused by PM2.5, which subsequently suppressing the expression of apoptotic regulatory protein and reducing the incidence of ovary apoptosis.

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Many tocopherols, one vitamin E.

Azzi A.

Mol Aspects Med. 2017 Jun 17. pii: S0098-2997(17)30041-9. doi: 10.1016/j.mam.2017.06.004. [Epub ahead of print]

Abstract

Four tocopherols are available in nature and are absorbed with the diet, but only one RRR-α-tocopherol satisfies the criteria of being a vitamin. The biological activity of the different tocopherols studied in the rat by the resorption-gestation test has been inconsistently extrapolated to human beings where the tocopherols have no influence on a successful pregnancy. Diminution of RRR-α-tocopherol intake results in diseases characterized by ataxia, whose pathogenetic mechanism, despite vigorous claims, has not been clarified. The calculation of the Daily Reference Intake (DRI), necessary to prevent disease, is based on an obsolete test, the peroxide-induced erythrocyte hemolysis, called the gold standard, but of highly questioned validity. If many epidemiological studies have given positive results, showing prevention by high vitamin E containing diets of cardiovascular events, neurodegenerative disease, macular degeneration and cancer, the clinical confirmatory intervention studies were mostly negative. On the positive side, besides preventing vitamin E deficiency diseases, vitamin E has shown efficacy as anti-inflammatory and immune boosting compound. It has also shown some efficacy in protecting against nonalcoholic hepato-steatosis. At a molecular level, vitamin E and some of its metabolites have shown capacity of regulating cell signaling and modulating gene transcription.

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Inflammatory and oxidative stress markers as indicator of atherogenesis in rats: antioxidants as preventive pharmacological methods.

Del Carmen Baez M, Tarán M, de La Paz Scribano M, Balceda A, Buonanotte C, Blencio S, Fonseca I, Moya M.

Antiinflamm Antiallergy Agents Med Chem. 2017 Jun 16. doi: 10.2174/1871523016666170616121133. [Epub ahead of print]

Abstract

The oxidative process in atherogenesis generated by proinflammatory induction and response to antioxidants vitamins in an experimental model were analyzed.

METHODS:

Male rats were used: (A)Control, (B)Control+vitamin E plus C, (C)Hyperfibrinogenemia and (D)Hyperfibrinogenemia+vitamins E plus C. Hyperfibrinogenemia induced by daily injection of adrenaline (0.1mg/day/rat) for 120 days.

TREATMENT:

3.42 mg/kg of vitamin E plus 2.14 mg/kg of vitamin C, fifteen days after induction. Vascular histology analyzed by optical microscopy. Fibrinogen, nitrites and superoxide dismutase(SOD) analyzed by spectrophotometry.

STATISTICS:

MANOVA, Hotelling test for post testing, significance level p<0.05.

RESULTS:

(C) group showed higher fibrinogen than (A) and (B)(p<0.001). Compared to (C) group, (D) showed a decrease of fibrinogen(p<0.001). A marked increase in nitrites was found in (C) versus (A), (B) and (D) groups(p<0.001). SOD activity increased in (C) group compared to groups (A) and (B) (p<0.001). In the group (D) an increase of the activity of this enzyme was observed in comparison to groups (C)(p<0.001), (A) and (B) (p<0.0001 in both). The (C) group shown endothelial denudation, thickening of the vascular intima and extracellular matrix enlargement with foam cells(p<0.001).

CONCLUSION:

These results strongly suggest that vitamins E plus C produce regression of inflammatory and oxidative stress processes in this experimental model.

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Vitamin E antagonizes ozone-induced asthma exacerbation in Balb/c mice through the Nrf2 pathway.

Duan L, Li J, Ma P, Yang X, Xu S.

Food Chem Toxicol. 2017 Jun 15;107(Pt A):47-56. doi: 10.1016/j.fct.2017.06.025. [Epub ahead of print]

Abstract

Millions of people are regularly exposed to ozone, a gas known to contribute significantly to worsening the symptoms of patients with asthma. However, the mechanisms underlying these ozone exacerbation effects are not fully understood. In this study, we examined the exacerbation effect of ozone in OVA-induced asthma mice and tried to demonstrate the protective mechanism of vitamin E (VE). An asthma mouse model was established, and used to identify the exacerbating effects of ozone by assessing cytokine and serum immunoglobulin concentrations, airway leukocyte infiltration, histopathological changes in lung tissues, and airway hyper-responsiveness. We then determined the amount of reactive oxygen species (ROS) accumulated, the extent to which VE induced ROS elimination, and examined the antagonistic effects of VE on the ozone-induced exacerbating effects. This study showed that 1-ppm ozone exposure could exacerbate OVA-induced asthma in mice. More importantly we found that ozone induced oxidative stress in asthmatic airways may lead to the inhibition of Nuclear factor-erythroid 2-related factor 2 (Nrf2), and may subsequently induce even more exaggerated oxidative stress associated with asthma exacerbation. Through VE induced Nrf2 activation and the subsequent increase in Nrf2 target protein expression, this study suggests a novel mechanism for alleviating ozone exacerbated asthma symptoms.

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Alzheimer Disease: Pharmacologic and Nonpharmacologic Therapies for Cognitive and Functional Symptoms.

Epperly T, Dunay MA, Boice JL.

Am Fam Physician. 2017 Jun 15;95(12):771-778.

Abstract

Alzheimer disease comprises a syndrome of progressive cognitive and functional decline. Treatments should target cognitive and functional symptoms. Cholinesterase inhibitors, memantine, and a combination of a cholinesterase inhibitor and memantine have produced statistically significant but clinically small delays in various domains of cognitive and functional decline in select patients with Alzheimer disease. Vitamin E has been shown to delay functional decline in patients with mild to moderate Alzheimer disease, especially when taken in combination with a cholinesterase inhibitor. Structured programs of physical exercise improve physical function and reduce rates of neuropsychiatric symptoms in patients with mild to severe Alzheimer disease. Cognitive stimulation programs show benefit in maintenance of cognitive function and improved self-reported quality of life in patients with mild to moderate Alzheimer disease.

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Vitamin E Modifies High-Fat Diet-Induced Increase of DNA Strand Breaks, and Changes in Expression and DNA Methylation of Dnmt1 and MLH1 in C57BL/6J Male Mice.

Remely M, Ferk F, Sterneder S, Setayesh T, Kepcija T, Roth S, Noorizadeh R, Greunz M, Rebhan I, Wagner KH, Knasmüller S, Haslberger A.

Nutrients. 2017 Jun 14;9(6). pii: E607. doi: 10.3390/nu9060607.

Abstract

Obesity is associated with low-grade inflammation, increased ROS production and DNA damage. Supplementation with antioxidants might ameliorate DNA damage and support epigenetic regulation of DNA repair. C57BL/6J male mice were fed a high-fat (HFD) or a control diet (CD) with and without vitamin E supplementation (4.5 mg/kg body weight (b.w.)) for four months. DNA damage, DNA promoter methylation and gene expression of Dnmt1 and a DNA repair gene (MLH1) were assayed in liver and colon. The HFD resulted in organ specific changes in DNA damage, the epigenetically important Dnmt1 gene, and the DNA repair gene MLH1. Vitamin E reduced DNA damage and showed organ-specific effects on MLH1 and Dnmt1 gene expression and methylation. These results suggest that interventions with antioxidants and epigenetic active food ingredients should be developed as an effective prevention for obesity-and oxidative stress-induced health risks.

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