Protective potential of Vitamin E against methylphenidate-induced male gonadal changes in albino rats.

Iqbal S, Hameed U, Hasan B, Zia-Ul-Islam, Ahmed M, Brohi AH

Int J Health Sci (Qassim). 2019 May-Jun;13(3):19-23.

Abstract

OBJECTIVE:

Attention deficit hyperactivity disorder ranks among the top neuropsychiatric disorder of childhood and adolescents. Methylphenidate (MPH) is the most frequently used pharmacologic agent to treat this condition. Its long-term use has been associated with many unwanted and adverse effects on many organs including male gonads, but so far no study has been done to find out a protective agent. This study investigated the protective potential of Vitamin E (Vit E) against the microscopic and morphometric alterations in male gonads induced by MPH, using albino rats.

METHODS:

Adult male albino rats were assigned into three equal groups including one control and two experimental groups. Experimental groups administered with MPH (10 mg/kg) and MPH (10 mg/kg) + Vit E orally (50 mg/kg), daily for 40 days. Testes of the sacrificed animals were removed, processed, and stained with hematoxylin and eosin for examining the microscopic and morphometric alterations and protective potential of Vit E. Data were analyzed using ANOVA.

RESULTS:

Experimental animals treated with MPH showed a significant decrease in the diameter of seminiferous tubules (296.86 ± 14.70 µm) and height of germinal epithelium (51.73 ± 3.15 µm) with a corresponding gain in the thickness of the interstitium (47.05 ± 4.94 µm). Animals treated with MPH + Vit E did not reveal any significant testicular microscopic changes and seminiferous tubular alterations induced by MPH.

CONCLUSION:

Vit E demonstrated a protective potential against the adverse changes induced by MPH in the male gonads in albino rats.

Malik A, Eggersdorfer M, Trilok-Kumar G

Int J Vitam Nutr Res. 2019 May 24:1-14. doi: 10.1024/0300-9831/a000590. [Epub ahead of print]

Abstract

Vitamin E is a lipid soluble antioxidant which mainly circulates as α-tocopherol in the human plasma. Its deficiency is associated with ataxia, neuropathy, anaemia and several other health conditions. Although substantial data on vitamin E status has been published worldwide, there is paucity of data on the extent of deficiency from most Asian countries, including India. Part of the problem is lack of validated biomarkers for vitamin E and no consensus on cut offs for defining deficiency and sufficiency. Thus, interpretation of the data on the vitamin E status is difficult. Limited available data from 31 studies on vitamin E status in healthy people from Asia, the most populated continent, has been collated for the purpose of this review. Broadly, the results suggest inadequate vitamin E status in most age groups, with the prevalence of deficiency reaching 67%, 80%, 56% and 72% in infants, children and adolescents, adults, elderly and pregnant women, respectively, based on varying cut offs. The findings are not surprising as both, vitamin E intakes and its status have not received too much attention in the past. Lack of conclusive data accentuates the need for more research on the vitamin E status across all age groups and to define age, gender and physiological state specific cut offs for vitamin E levels.

Hakiminia B, Goudarzi A, Moghaddas A

J Biochem Mol Toxicol. 2019 May 21:e22349. doi: 10.1002/jbt.22349. [Epub ahead of print]

Abstract

Cisplatin is one of the highly consumed and effective antitumor agents whose clinical application is accompanied by nephrotoxicity adverse reaction. Also, other complications such as ototoxicity and hepatotoxicity are a matter of concern. Today, it is suggested that cisplatin-associated toxicities are mainly induced by free radicals production, which will result in oxidative organ injury. The evidence is growing over the protective effects of antioxidants on cisplatin-induced adverse reactions especially nephrotoxicity. The possible protective effects of vitamin E and its derivative in cisplatin-induced nephrotoxicity and ototoxicity are reviewed here at the light of pertinent results from basic and clinical research. Administration of vitamin E alone or in combination with other antioxidant agents could cause amelioration in oxidative stress biomarkers such as decreasing the level of malondialdehyde, reducing serum urea and creatinine, and also enhancing the activities of renal antioxidant enzymes including renal catalase, glutathione-S-transferase, and superoxide dismutase. Although the data from most of the studies are in favors of protective effects of vitamin E against cisplatin-induced toxicity, more clinical trials are needed to clarify the clinical importance of vitamin E administration as an antioxidant during cisplatin therapy in cancer condition.

Huang J, Weinstein SJ, Yu K, Männistö S, Albanes D

J Natl Cancer Inst. 2019 May 11. pii: djz077. doi: 10.1093/jnci/djz077. [Epub ahead of print]

Abstract

BACKGROUND:

Epidemiologic data are inconsistent regarding the vitamin E-lung cancer association, and no study has examined serologic changes in vitamin E status in relation to subsequent risk.

METHODS:

In a cohort of 22,781 male smokers in the ATBC Study, we ascertained 3,184 lung cancer cases during up to 28 years of observation. Cox proportional hazards models examined whether higher serum alpha-tocopherol concentrations at baseline, 3 years, or the interval change were associated with lower lung cancer risk. All statistical tests were two-sided.

RESULTS:

After adjustment for age, body mass index, smoking intensity and duration, serum total cholesterol, and trial intervention group, we found lower lung cancer risk in men with high baseline alpha-tocopherol (5th quintile (Q5) vs Q1, hazard ratio (HR)=0.76, 95%CI =0.66 to 0.87; Ptrend<0.001). A similar reduction in risk was seen for serum alpha-tocopherol at 3 years (Q5 vs Q1, HR = 0.78, 95%CI =0.67 to 0.91; Ptrend=0.004). The inverse risk association appeared stronger for younger men and those having smoked fewer years, but was similar across trial intervention groups. We also found reduced risk among un-supplemented men with a lower serum alpha-tocopherol at baseline who had greater increases in concentrations at 3 years (3rd tertile vs 1st tertile of serum alpha-tocopherol change, HR = 0.74, 95% CI = 0.59 to 0.91, P=0.005).

CONCLUSION:

Higher vitamin E status, as measured by serum alpha-tocopherol concentration, as well as repletion of a low vitamin E state, was related to decreased lung cancer risk during a 28-year period. Our findings provide evidence supporting the importance of adequate physiological vitamin E status for lung cancer risk reduction.

Ranard KM, Kuchan MJ, Erdman JW Jr

Lipids. 2019 May;54(5):289-299. doi: 10.1002/lipd.12149. Epub 2019 Apr 16.

Abstract

Of the antioxidant vitamin E isoforms, α-tocopherol (αT) and γ-tocopherol (γT) are the most abundant in the human diet, and αT is consumed from both natural and synthetic sources. αT and γT may differentially impact inflammation and influence cardiovascular outcomes, in part by modulating gene expression. The goal of this study was to compare the effects of natural αT, synthetic αT, and γT on gene expression in two human cell lines. Human aortic smooth muscle cells (HASMC) and endothelial cells (HAEC) were either: (1) treated with 25 μM tocopherolsalone, or (2) pretreated with tocopherols prior to a pro-inflammatory cytokine (tumor necrosis factor-alpha, TNF-α) stimulation. The expression of atherosclerosis-related genes was measured using RT² Profiler PCR arrays. Tocopherol treatments alone did not significantly modulate the expression of genes in unstimulated HASMC or HAEC. TNF-α stimulation significantly upregulated genes involved with apoptosis and stress response in both cell lines. Pretreating cells with tocopherols did not normalize the gene expression changes induced by TNF-α. However, αT pretreatments, but not γT pretreatments, attenuated TNF expression in both HASMC and HAEC. These findings suggest that under stimulated conditions, αT modestly modulates the expression of selective genes and that αT may be more anti-inflammatory than γT.

Li D, Tang H, Wei P, Zheng J, Daniel CR, Hassan MM

J Nutr. 2019 May 17. pii: nxz081. doi: 10.1093/jn/nxz081. [Epub ahead of print]

Abstract

BACKGROUND:

Previous studies have found that meat-derived mutagens increase, and vitamin C or E decrease, the risk of pancreatic cancer.

OBJECTIVE:

The aim of this study was to determine whether intake of vitamin C or E modulates the association between meat-derived mutagen exposure and risk of pancreatic cancer.

DESIGN:

We conducted a case-control study in 1321 patients with pathologically confirmed pancreatic ductal adenocarcinoma (PDAC) and 1061 healthy controls (aged 28-88 y). Cases and controls were frequency-matched by age, sex, and race/ethnicity. Mutagen intake was assessed using a meat preparation questionnaire. Intakes of vitamin C, E, and other dietary components were assessed via a food-frequency questionnaire in a subset of 811 cases and 818 controls. ORs and 95% CIs were estimated in multivariable-adjusted logistic regression models.

RESULTS:

The risk of PDAC was not associated with meat intake but was associated with consumption of well-done grilled or barbecued chicken (OR: 1.57; 95% CI: 1.18, 2.09; P = 0.001). Intake of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline was associated with increased PDAC risk (Ptrend = 0.047). Participants in the highest, as compared with the lowest, quintile of 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (PhIP) intake experienced a 38% increased risk of PDAC (95% CI: 1.00, 1.90; P = 0.048). Intakes of total vitamin C or E from food and supplements or from supplements alone were each inversely associated with PDAC risk. Stratified analyses showed differential associations for PhIP intake and PDAC risk, such that risk increased among individuals with lower intake of vitamin C or E and decreased among those with higher vitamin intake. Significant interactions of dietary vitamin C, dietary vitamin E, and total vitamin E with PhIP intake were detected (Pinteraction = 0.023, <0.001, and 0.013, respectively).

CONCLUSIONS:

Consistent with experimental evidence, this study of 811 cases and 818 controls has shown that high intake of dietary vitamin C or E mitigates the risk of PhIP-related PDAC.

Alghadir AH, Gabr SA, Iqbal ZA, Al-Eisa E

BMC Pediatr. 2019 May 17;19(1):156. doi: 10.1186/s12887-019-1528-1.

Abstract

BACKGROUND:

Although various studies have shown the effect of vigorous physical activity on academic achievements, no studies have investigated the effect of vitamin E levels on academic performance. The present study aimed to assess the association between physical activity, vitamin E levels and total antioxidant capacity on the academic performance and executive functions of adolescents aged 15-18 years.

METHODS:

The physical activity of participants was assessed according to the time spent engaging in moderate and intense exercise programs. Participants were classified into three groups representing mild, moderate, and high activity. Serum total antioxidant capacity was measured using a colorimetric assay kit. Vitamin E was estimated by the α- and γ-tocopherol levels in fasting serum samples using high-performance liquid chromatography paired with a diode array detector. School grades (ranging from 1.0, very poor; to 10.0, outstanding) were obtained at the end of the academic year to evaluate academic performance and executive functions.

RESULTS:

A total of 120 school students (mean age 16.36 ± 0.77 years; 70 boys, 50 girls) participated in the study. Academic performance was higher for students classified as moderately or highly active compared with those in the mild activity group. Serum levels of vitamin E, total antioxidant capacity, and leisure-time physical activity were also higher in the moderate and high activity groups. There was a significant correlation between age, gender, body mind index, α- and γ-tocopherol, total antioxidant capacity, leisure-time physical activity and academic performance.

CONCLUSIONS:

The academic performance and executive function scores were found to be positively correlated with age, gender, α- and γ-tocopherol, total antioxidant capacity, and physical activity; and were negatively correlated with body mind index. Our findings indicate that physical activity should be promoted during and after school hours, along with a healthy balanced diet including vitamin E.

Chiricosta L, Gugliandolo A, Tardiolo G, Bramanti P, Mazzon E

Nutrients. 2019 May 15;11(5). pii: E1081. doi: 10.3390/nu11051081.

Abstract

Vitamin E family is composed of different tocopherols and tocotrienols that are well-known as antioxidants but that exert also non-antioxidant effects. Oxidative stress may be involved in the progression of neurodegenerative disorders including amyotrophic lateral sclerosis (ALS), characterized by motor neuron death. The aim of the study was the evaluation of the changes induced in the transcriptional profile of NSC-34 motor neurons treated with α-tocopherol. In particular, cells were treated for 24 h with 10 µM α-tocopherol, RNA was extracted and transcriptomic analysis was performed using Next Generation Sequencing. Vitamin E treatment modulated MAPK signaling pathway. The evaluation revealed that 34 and 12 genes, respectively belonging to “Classical MAP kinase pathway” and “JNK and p38 MAP kinase pathway”, were involved. In particular, a downregulation of the genes encoding for p38 (Log₂ fold change -0.87 and -0.67) and JNK (Log₂ fold change -0.16) was found. On the contrary, the gene encoding for ERK showed a higher expression in cells treated with vitamin E (Log₂ fold change 0.30). Since p38 and JNK seem more involved in cell death, while ERK in cell survival, the data suggested that vitamin E treatment may exert a protective role in NSC-34 motor neurons. Moreover, Vitamin E treatment reduced the expression of the genes which encode proteins involved in mitophagy. These results indicate that vitamin E may be an efficacious therapy in preventing motor neuron death, opening new strategies for those diseases that involve motor neurons, including ALS.