α-Tocopherol Depletion Exacerbates Lipopolysaccharide-Induced Reduction of Grip Strength.

Background: α-Tocopherol (αT) deficiency causes several neurologic disorders, such as spinocerebellar ataxia, peripheral neuropathy, and myopathy. Furthermore, decreased antibody production, impaired ex vivo T cell function, and elevated cytokine production are observed in humans and mice with αT deficiency. Although modeling αT deficiency in animals is challenging, αT depletion can be more readily achieved in α-tocopherol transfer protein-null (Ttpa) mice than wild-type (WT) mice.

α-Tocopherol Transfer Protein-Null Mice with Very Low α-Tocopherol Status Do Not Have an Enhanced Lipopolysaccharide-Induced Acute Inflammatory Response.

Background: The α-tocopherol transfer protein-null () mouse model is a valuable tool for studying the molecular and functional consequences of vitamin E (α-tocopherol, αT) deficiency. Because αT has been associated with reduced oxidative stress and improved immune function, we hypothesized that depleted αT concentration would exacerbate LPS-induced acute inflammatory response in the brain and heart of mice fed a vitamin E deficient (VED) diet.

Objectives: The objective was to investigate how extremely low αT status, followed by exposure to LPS, altered the acute inflammatory response to LPS in and wild-type () mice.