Fusarium mycotoxins are one of the largest families of mycotoxins. Among these mycotoxins, deoxynivalenol is the most widespread pollutant of grains. However, the mechanism underlying the effect of deoxynivalenol on cytotoxicity in human brain endothelial cells was still unclear. This study examined whether deoxynivalenol induced oxidative stress-associated cytotoxicity in primary human brain endothelial cells (HBEC-5i), and explored whether Vitamin E (VE), a selective antioxidant, had protective effects on deoxynivalenol-treated cells. Deoxynivalenol (10-50 μM) concentration-dependently induced cytotoxicity in HBEC-5i cells. Deoxynivalenol (IC50 = 20 μM) activated mitochondrial apoptotic pathway by modulating antioxidant protein expressions (Nrf2, HO-1 and NQO1). More significantly, pre-treatment with VE (20 μM) attenuated the deoxynivalenol-induced cytotoxicity in this cell model. Together, VE significantly alleviated the apoptotic effects of deoxynivalenol in HBEC-5i cells suggesting that it protected the cells against deoxynivalenol-induced oxidative damage. Our findings provided new insight that VE had the potential to ameliorate neurotoxicity of deoxynivalenol.

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Vitamin E comprises 8 fat-soluble isoforms: α-, β-, γ-, and δ-tocopherol and α-, β-, γ-, and δ-tocotrienol. Yet the body preferentially uses α-tocopherol, and only α-tocopherol supplementation can reverse vitamin E deficiency symptoms. However, other isoforms influence many biological functions in the body, including inflammation and stress. Therefore, the study objective was to determine metabolic and performance responses in young calves fed diets containing a constant amount of α-tocopherol and increasing amounts of soybean oil-derived mixed γ- and δ-tocopherols. Holstein calves [n = 48; 2-3 d of age; 40.2 kg of initial body weight (BW), standard error = 0.54] were assigned to receive approximately 0, 5, 10, or 15 mg/kg of BW daily (treatments T0, T1, T2, and T3, respectively) of mixed tocopherols (TMIX) provided in milk replacer (MR) and calf starter. The TMIX liquid contained 86% γδ-tocopherols and 9% α-tocopherol. Milk replacers were formulated to contain approximately 0, 400, 800, or 1,200 mg of TMIX/kg for treatments T0, T1, T2, and T3, respectively. Calf starters were formulated to contain approximately 0, 250, 500, or 750 mg of TMIX/kg for treatments T0, T1, T2, and T3, respectively. Mean consumption of γδ-tocopherols was 0.0, 6.5, 14.3, and 20.5 mg/kg of BW, respectively. Milk replacer contained 24% crude protein (CP) and 20% fat on a dry matter (DM) basis. Calf starters were pelleted and offered for ad libitum consumption from 0 to 56 d. Starters contained 18 to 20% CP and 9 to 12% starch in the DM. On d 28, 4 calves per treatment were randomly selected for slaughter, and necropsy was performed. Samples of liver, duodenum, ileum, and trapezius muscle were collected and stored before analysis for α-, β-, γ-, and δ-tocopherols and δ-tocotrienol. Data were analyzed using a completely randomized design using mixed model ANOVA with orthogonal polynomials to determine linear and quadratic effects of TMIX. Repeated-measures analyses were performed for data collected over time. Increasing dietary TMIX increased or tended to increase change in hip width at 28 and 56 d, respectively, and improved average daily BW gain and gain-to-feed ratio at 56 d. Increasing TMIX reduced plasma xanthine oxidase at 0 h and tended to reduce concentrations at 24 h following vaccination with 2 commercial vaccines on d 28; however, we detected no effect of TMIX following vaccination on d 56. Concentration of α-tocopherol in skeletal muscle declined quadratically with increasing TMIX, whereas ileal and liver γ-tocopherol increased linearly with increasing TMIX. The number of mucin-2 cells in the ileum increased more than 2-fold in calves fed T3. Addition of mixed tocopherols to diets of young dairy calves improved animal growth and altered indices of antioxidant metabolism.

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This study aims to evaluate the influence of Vitamin A and E homologues toward acrylamide in equimolar asparagine-glucose model system. Vitamin A homologue as β-carotene (BC) and five Vitamin E homologues, i.e., α-tocopherol (AT), δ-tocopherol (DT), α-tocotrienol (ATT), γ-tocotrienol (GTT), and δ-tocotrienol (DTT), were tested at different concentrations (1 and 10 µmol) and subjected to heating at 160 °C for 20 min before acrylamide quantification. At lower concentrations (1 µmol; 431, 403, 411 ppm, respectively), AT, DT, and GTT significantly increase acrylamide. Except for DT, enhancing concentration to 10 µmol (5370, 4310, 4250, 3970, and 4110 ppm, respectively) caused significant acrylamide formation. From linear regression model, acrylamide concentration demonstrated significant depreciation over concentration increase in AT (Beta = -83.0, R² = 0.652, p ≤ 0.05) and DT (Beta = -71.6, R² = 0.930, p ≤ 0.05). This study indicates that different Vitamin A and E homologue concentrations could determine their functionality either as antioxidants or pro-oxidants.

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Reinforcement of the body with exogenous antioxidants have been shown to mitigate the negative effects of African trypanosomiasis on the host and contribute greatly to their survival. This study was therefore conducted to evaluate the effects of oral administration of Vitamin E on the early stage of Trypanosoma brucei brucei infection. To achieve this, parasite free healthy rats were acclimatized for 2 weeks before they were divided into three groups. Two of the groups were infected by intraperitoneal inoculation of 1 × 10⁴ parasites/rat and monitored for the presence of Trypanosoma brucei brucei. Blood samples were collected from the infected rats from the second day post infection to detect the presence of parasites. Vitamin E treatment started day 4 post infection at the onset of parasitaemia. Parasites were monitored till the end of the study. The blood glucose level was determined using a glucometer; the lipid profile, liver and kidney biomarkers, electrolytes and protein were determined by colorimetric method using commercial kits. Haematological parameters were analysed using a sysmex haematology analyser. The results of this study showed that the infection adversely affected the biomarkers examined showing its negative effect on liver, kidney, haematological parameters and host electrolyte balance. Treatments with Vitamin E was however able to mitigate the negative effect of this infection. In conclusion, the treatment was able to ameliorate the anaemia and organ damage caused by Trypanosoma brucei brucei, extend the life span of the treated rats and greatly delay the time taken to get to the second stage of the infection.

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Vitamin E is a potent antioxidant that helps to counteract oxidative stress in the body. Oxidative stress is known to greatly affect people living with HIV (PLWH) through the stimulation of HIV replication and apoptosis of CD4+ T cells. There is however, a paucity of scientific data on the serum levels of vitamin E among PLWH in Ghana, and hence, there is a need to assess its level because of the pivotal role it plays in cell longevity determination and the immune system enhancement of such persons. This study aims to assess the serum levels of vitamin E among PLWH undergoing highly active antiretroviral therapy at Ho Teaching Hospital, Ghana. In a cross-sectional study, serum vitamin E levels of 103 randomly selected PLWH aged 24-88 years who attended an antiretroviral therapy clinic at the Ho Teaching Hospital, Ghana, were measured by following standard protocols. A 24-hour dietary recall and food frequency questionnaire were employed to assess dietary intake. The results show that a high level of serum vitamin E deficiency (82.5%) was observed among the participants. Majority (91.3%) of the participants had normal serum zinc status. Participants’ serum vitamin E levels did not show significant correlation with their dietary intakes (correlation coefficient (ρ) = -0.094, p-value = 0.35). The prevalence of vitamin E deficiency among underweight, normal weight, overweight, and obese participants was 91.7%, 75.4%, 86.5%, and 91.7% respectively with no significant difference among these groups. There was no significant correlation between serum vitamin E levels and HIV infection duration (ρ = 0.010, p-value = 0.405) and HAART duration (ρ = 0.001, p-value = 0.313). The low serum vitamin E levels found in this study suggests that the participants could potentially be at an increased risk of developing oxidative stress and its effects.

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