Ranard Katherine M, Kuchan Matthew J, Juraska Janice M, Erdman John W
Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Champaign, IL, USA.
Abbott Nutrition, Columbus, OH, USA.
Curr Dev Nutr. 2021 Feb 12;5(3):nzab008. doi: 10.1093/cdn/nzab008. eCollection 2021 Mar.
Vitamin E (α-tocopherol, α-T) deficiency causes neurological pathologies. α-T supplementation improves outcomes, but the relative bioactivities of dietary natural and synthetic α-T in neural tissues are unknown.
The aim was to assess the effects of dietary α-T source and dose on oxidative stress and myelination in adult α-tocopherol transfer protein-null ( ) mouse cerebellum and spinal cord.
Three-week-old male mice ( = 56) were fed 1 of 4 AIN-93G-based diets for 37 wk: vitamin E-deficient (VED; below α-T limit of detection); natural α-T, 600 mg/kg diet (NAT); synthetic α-T, 816 mg/kg diet (SYN); or high synthetic α-T, 1200 mg/kg diet (HSYN). Male littermates ( = 14) fed AIN-93G (75 mg synthetic α-T/kg diet; CON) served as controls. At 40 wk of age, total and stereoisomer α-T concentrations and oxidative stress markers were determined ( = 7/group). Cerebellar Purkinje neuron morphology and white matter areas in cerebellum and spinal cord were assessed in a second subset of animals ( = 7/group).
Cerebral cortex α-T concentrations were undetectable in mice fed the VED diet. α-T concentrations were increased in NAT (4.6 ± 0.3 nmol/g), SYN (8.0 ± 0.7 nmol/g), and HSYN (8.5 ± 0.3 nmol/g) mice, but were significantly lower than in mice fed CON (27.8 ± 1.9 nmol/g) ( < 0.001). stereoisomers constituted the majority of α-T in brains of mice (91%) and mice fed NAT (100%), but were substantially lower in the SYN and HSYN groups (∼53%). Neuroinflammatory genes were increased in the spinal cord, but not cerebellum, of VED-fed animals; NAT, SYN, and HSYN normalized their expression. Cerebellar Purkinje neuron atrophy and myelin pathologies were not visible in mice.
Natural and synthetic α-T supplementation normalized neuroinflammatory markers in neural tissues of 10-mo-old mice. α-T prevents tissue-specific molecular abnormalities, which may prevent severe morphological changes during late adulthood.
维生素E（α-生育酚，α-T）缺乏会导致神经病理学变化。补充α-T可改善预后，但膳食中天然和合成α-T在神经组织中的相对生物活性尚不清楚。
评估膳食α-T来源和剂量对成年α-生育酚转运蛋白缺失（ ）小鼠小脑和脊髓氧化应激及髓鞘形成的影响。
将3周龄雄性 小鼠（ = 56）喂食4种基于AIN-93G的日粮中的1种，持续37周：维生素E缺乏（VED；低于α-T检测限）；天然α-T，600 mg/kg日粮（NAT）；合成α-T，816 mg/kg日粮（SYN）；或高剂量合成α-T，1200 mg/kg日粮（HSYN）。喂食AIN-93G（75 mg合成α-T/kg日粮；CON）的雄性 同窝小鼠（ = 14）作为对照。40周龄时，测定总α-T和立体异构体α-T浓度以及氧化应激标志物（每组 = 7）。在另一组动物中评估小脑浦肯野神经元形态以及小脑和脊髓中的白质区域（每组 = 7）。
喂食VED日粮的 小鼠大脑皮质中α-T浓度无法检测到。NAT组（4.6 ± 0.3 nmol/g）、SYN组（8.0 ± 0.7 nmol/g）和HSYN组（8.5 ± 0.3 nmol/g）小鼠的α-T浓度升高，但显著低于喂食CON的 小鼠（27.8 ± 1.9 nmol/g）（ < 0.001）。 立体异构体在 小鼠（91%）和喂食NAT的 小鼠（100%）大脑中的α-T中占大多数，但在SYN组和HSYN组中显著降低（约53%）。喂食VED的动物脊髓中神经炎症基因增加，但小脑中未增加；NAT、SYN和HSYN组使其表达恢复正常。 小鼠小脑中未见浦肯野神经元萎缩和髓鞘病变。
天然和合成α-T补充使10月龄 小鼠神经组织中的神经炎症标志物恢复正常。α-T可预防组织特异性分子异常，这可能预防成年后期的严重形态学变化。
