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.

Read More

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.

Read More