Efficacy of vitamins E and C for reversing the cytotoxic effects of nicotine and cotinine.

Torshabi M, Rezaei Esfahrood Z, Jamshidi M, Mansuri Torshizi A, Sotoudeh S

Eur J Oral Sci. 2017 Dec;125(6):426-437. doi: 10.1111/eos.12375. Epub 2017 Oct 12.

Abstract

Nicotine has adverse cellular and molecular effects on oral mucosa, bone, and teeth. Vitamin E (α-tocopherol) and vitamin C (ascorbic acid) are biological antioxidants with positive effects on wound healing and bone formation. This in vitro study sought to assess the cytotoxic effects of different concentrations of nicotine and cotinine (a metabolite of nicotine) on MG-63 osteoblast-like cells and human gingival fibroblasts (HGFs) in the presence and absence of antioxidant vitamins E and C (separately and combined). Cell viability and proliferation were assessed using the methyl thiazol tetrazolium (MTT) assay. Cell migration was assessed using the scratch test, and expression of apoptosis-related genes was quantitatively analyzed using real-time PCR. Dose-dependent negative effects of nicotine on the morphology, viability, proliferation, and migration of MG-63 and HGF cells were statistically significantly greater than those of cotinine. Vitamin E (separately and combined with vitamin C) was statistically significantly more effective than vitamin C (at the concentration used in this study) at improving cell viability, proliferation, and migration, and at reducing apoptosis of cells exposed to nicotine or cotinine. Based on the positive results of this study, vitamin C and especially vitamin E (systemically and/or locally) may be useful in the repair and regeneration of oral hard and soft tissues in smokers.

Clemente-Suárez VJ, Mielgo-Ayuso J, Quiles JL, Varela-Lopez A, Aranda P

Physiol Int. 2017 Dec 1;104(4):291-300. doi: 10.1556/2060.104.2017.4.2.

Abstract

This study was aimed to analyze the effect of two different megadoses of α-tocopherol (vit E) in the antioxidant activity and red and white blood series of Wistar rats after a 180-min ultraendurance probe. Three groups of 10 rats were analyzed; VEAG: acute administration of a megadoses of 5,000 IU/kg of vit E the day before the probe; VECG: chronic administration of 1,000 IU/kg/day of vit E for 6 days before the probe; CG: placebo administration. VEAG presented white cells, red blood cells, hematocrit, hemoglobin values significantly higher than CG and VECG (p < 0.05). The mean corpuscular hemoglobin and lymphocytes concentrations were significantly higher in the VECG than in the other two groups (p < 0.05). Similarly, VEAG presented a significantly higher vit E blood concentration than VECG and CG (p < 0.05), and VECG than CG (p < 0.05). Finally, we found a significantly positive correlation between trolox equivalent antioxidant capacity (TEAC) and red blood cells concentration (r = 0.374) and a significantly inverse correlation between TEAC and blood lactate concentration (r = -0.365). Our findings suggest that acute vit E megadoses could protect against transitory sport anemia symptoms and increase the white blood cell count in comparison with the chronic dose and control groups after an ultraendurance probe.

Abedi Z, Khaza'ai H, Vidyadaran S, Mutalib MSA

Biomedicines. 2017 Dec 1;5(4). pii: E68. doi: 10.3390/biomedicines5040068.

Abstract

Astrocytes are known as structural and supporting cells in the central nervous system (CNS). Glutamate, as a main excitatory amino acid neurotransmitter in the mammalian central nervous system, can be excitotoxic, playing a key role in many chronic neurodegenerative diseases. The aim of the current study was to elucidate the potential of vitamin E in protecting glutamate-injured primary astrocytes. Hence, primary astrocytes were isolated from mixed glial cells of C57BL/6 mice by applying the EasySep^® Mouse CD11b Positive Selection Kit, cultured in Dulbecco’s modified Eagle medium (DMEM) and supplemented with special nutrients. The IC₂₀ and IC₅₀ values of glutamate, as well as the cell viability of primary astrocytes, were assessed with 100 ng/mL, 200 ng/mL, and 300 ng/mL of tocotrienol-rich fraction (TRF) and alpha-tocopherol (α-TCP), as determined by an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The mitochondrial membrane potential (MMP) detected in primary astrocytes was assessed with the same concentrations of TRF and α-TCP. The expression levels of the ionotropic glutamate receptor genes (Gria2, Grin2A, GRIK1) were independently determined using RT-PCR. The purification rate of astrocytes was measured by a flow-cytometer as circa 79.4%. The IC₂₀ and IC₅₀ values of glutamate were determined as 10 mM and 100 mM, respectively. Exposure to 100 mM of glutamate in primary astrocytes caused the inhibition of cell viability of approximately 64.75% and 61.10% in pre- and post-study, respectively (p < 0.05). Both TRF and α-TCP (at the lowest and highest concentrations, respectively) were able to increase the MMP to 88.46% and 93.31% pre-treatment, and 78.43% and 81.22% post-treatment, respectively. Additionally, the findings showed a similar pattern for the expression level of the ionotropic glutamate receptor genes. Increased extracellular calcium concentrations were also observed, indicating that the presence of vitamin E altered the polarization of astrocytes. In conclusion, α-TCP showed better recovery and prophylactic effects as compared to TRF in the pre-treatment of glutamate-injured primary astrocytes.

Yang F, Wolk A, Håkansson N, Pedersen NL, Wirdefeldt K

Mov Disord. 2017 Nov;32(11):1631-1636. doi: 10.1002/mds.27120. Epub 2017 Sep 7.

Abstract

BACKGROUND:

A neuroprotective effect of dietary antioxidants on Parkinson’s disease (PD) risk has been suggested, but epidemiological evidence is limited.

OBJECTIVES:

To examine the associations between intake of dietary antioxidant vitamins and total antioxidant capacity and risk of PD.

METHODS:

We prospectively assessed the relationships of dietary antioxidant vitamins C and E, ß-carotene, and total antioxidant capacity with PD risk in two population-based cohorts (38,937 women and 45,837 men).

RESULTS:

During a mean 14.9-year follow-up period, 1,329 PD cases were identified. Dietary intake of ß-carotene was associated with a lower risk of PD (hazard ratio: 0.86; 95% confidence interval: 0.78-0.95; P_trend < 0.01 for women and hazard ratio: 0.91; 95% confidence interval: 0.84-0.99; P_trend = 0.05 for men). An inverse association between dietary vitamin E and PD risk was found in women (hazard ratio: 0.87; 95% confidence interval: 0.79-0.96; P_trend = 0.02). Dietary intake of vitamin C was inversely associated with PD risk in women at borderline significance (hazard ratio: 0.91; 95% confidence interval: 0.83-1.00; P_trend = 0.04). There was no association between dietary total antioxidant capacity and PD risk in either women (hazard ratio: 0.93; 95% confidence interval: 0.84-1.02; P_trend = 0.35) or men (hazard ratio: 1.00; 95% confidence interval: 0.93-1.07; P_trend = 0.97).

CONCLUSION:

Intake of dietary vitamin E and ß-carotene was associated with a lower risk of PD.

Zhang J, Song W, Sun Y, Shan A

Environ Sci Pollut Res Int. 2017 Nov;24(32):24916-24927. doi: 10.1007/s11356-017-0104-1.

Abstract

Currently, public pay more attention to the adverse effect of organophosphate pesticides on human and animal health and on the environment in developing nations. Vitamin E may protect the hepatocyte and increase the function of liver. The study was to investigate the effects of phoxim-induced hepatotoxicity on Sprague Dawley (SD) rats and the protection of vitamin E. SD rats received by gavage 180 mg kg^-1 (per body weight) of phoxim, 200 mg kg^-1 (per body weight) of vitamin E, and phoxim + vitamin E. The results showed that exposure to phoxim elevated liver coefficient; glutamyl transpeptidase (GGT), aspartate aminotransferase, alkaline phosphatase, total bilirubin, total bile acid, and alanine aminotransferase in the serum; ROS in the liver; and the expression of p53, Bax, CYP2E1, ROS, caspase-9, caspase-8, and caspase-3, while phoxim caused a reduction of total protein, albumin, and cholinesterase in the serum; acetylcholinesterase, total antioxidant capacity, glutathione peroxidase, and glutathione in the liver; and the expression of Bcl-2. Vitamin Emodified the phoxim-induced hepatotoxicity by reducing the GGT in the serum, malondialdehyde in the liver, and the expression of CYP2E1 significantly. There were no significant changes of globulin in the serum, the activity of catalase in the liver, as well as expression levels of Fas and Bad in the liver. Overall, subacute exposure to phoxim induced hepatic injury, oxidative stress damage, and cell apoptosis. Vitamin Emodified phoxim-induced hepatotoxicity slightly. And, vitamin E minimized oxidative stress damage and ultrastructural changes in rat hepatocytes notably.

Mâncio RD, Hermes TA, Macedo AB, Mizobuti DS, Valduga AH, Rupcic IF, Minatel E

Nutrition. 2017 Nov - Dec;43-44:39-46. doi: 10.1016/j.nut.2017.07.003.

Abstract

OBJECTIVE:

Oxidative stress, in addition to the absence of the dystrophin protein, has been considered an important regulator of Duchenne muscular dystrophy (DMD). Vitamin E presents an important role as a potent antioxidant and in preserving the integrity of the cell membrane. In this study, we evaluated the effects of vitamin E therapy on some physiological pathways that can contribute to muscle injury in the diaphragm muscle of mdx mice (the experimental model of DMD) such as CK levels, inflammatory response, oxidative stress, and the enzymatic antioxidant system.

METHODS:

Mdx mice (14 d old) received 40 mg vitamin E/kg daily by oral gavage for 14 d, followed by the removal of the diaphragm muscle. Control mdx mice and C57BL/10 mice received saline only for the same period and were used as controls.

RESULTS:

Vitamin E reduced the muscle fiber damage, oxidative stress, and inflammation process in the diaphragm muscle of mdx mice.

CONCLUSIONS:

Vitamin E improves skeletal muscle injury in mdx mice, promoting membrane repair and exhibiting antioxidant and antiinflammatory effects. These vitamin E effects suggest that this antioxidant therapy may be a relevant approach for dystrophinopathies.

Blaha V, Blaha M, Solichová D, Krčmová LK, Lánská M, Havel E, Vyroubal P, Zadák Z, Žák P, Sobotka L

Atheroscler Suppl. 2017 Nov;30:159-165. doi: 10.1016/j.atherosclerosissup.2017.05.002.

Abstract

Oxidative stress is thought to play an important role in the pathogenesis of disorders associated with atherosclerosis. Alpha-tocopherol is considered to be an effective lipophilic antioxidant, which protects lipid membranes against peroxidation and thus prevents cell damage by reaction with free radicals. However, measurement of alpha-tocopherol concentration in serum does not reflect the content of α-tocopherol in membranes whereas erythrocyte alpha-tocopherol may be good indicator of antioxidative status. Therefore a simple isocratic reversed phase HPLC method has been developed and validated for the determination of alpha-tocopherol in human erythrocytes in a clinical setting. The content of alpha-tocopherol in human erythrocyte membrane and lipoperoxidation were studied in patients with severe hypercholesterolemia treated by lipoprotein apheresis. The group of hypercholesterolemic patients (n = 14) treated by lipoprotein apheresis was compared to healthy adult normolipidemic controls. After lipoprotein apheresis, the content of in membrane alpha-tocopherol did not change significantly despite decreased tocopherol in serum and lipoprotein fractions. We observed significantly decreased lipoperoxidation as revealed by serum TBARS, representing end products of lipid peroxidation, which increased from third day afterwards and remained significantly higher in comparison to controls until the next LDL-apheresis. We conclude that aggressive lipid lowering procedure with lipoprotein apheresis was associated with favorable transient decrease of lipoperoxidation. Simultaneously the cell membrane bound antioxidative defense mechanisms as reflected by the content of alpha-tocopherol in human erythrocyte membrane where not depressed in spite of its decreased plasma lipid carrier. Another variables involved remain to be investigated.