Effects on neural function of repleting vitamin E-deficient rats with alpha-tocopherol.

J Neurophysiol

Biochemistry, Endocrinology and Metabolism Unit, Institute of Child Health, University College London, London, United Kingdom.

Published: April 2006

A severe and chronic deficiency of vitamin E (alpha-tocopherol) is associated with a characteristic neurological syndrome with typical "clinical," neuropathological, and electrophysiological abnormalities in both humans and experimental animals. Repletion of vitamin E-deficient human subjects with alpha-tocopherol typically halts the progression of the neural signs and symptoms, and in some cases, can result in objective improvement. Electrophysiological parameters provide an objective measure of neural and visual function and improvement of some of these measures has been reported after repletion with vitamin E in humans. In this longitudinal study, the effects of repleting rats with a diet containing 36 mg/kg all-rac-alpha-tocopheryl acetate for 20 wk after they had been receiving a vitamin E-deficient diet for 38 wk was studied. We report significant improvements in growth and a number of electrophysiological parameters of both neural and visual function after repletion. These results confirm the validity of the vitamin E-deficient rat as a model of vitamin E deficiency in humans.

Download full-text PDF

Source
http://dx.doi.org/10.1152/jn.00842.2005DOI Listing

Publication Analysis

Top Keywords

vitamin e-deficient
16
repletion vitamin
8
electrophysiological parameters
8
neural visual
8
visual function
8
vitamin
7
effects neural
4
neural function
4
function repleting
4
repleting vitamin
4

Similar Publications

Introduction Children with cystic fibrosis (CF) have lipid maldigestion due to pancreatic insufficiency, which causes malabsorption of fat-soluble vitamins. The primary objective of this study was to assess the prevalence of vitamin E deficiency among children with CF. The secondary objective was to examine the correlation between vitamin E levels with demographic data, laboratory findings, and the number of pulmonary exacerbations.

View Article and Find Full Text PDF
Article Synopsis
  • Vascular calcification contributes to cardiovascular disease by rupturing vulnerable atherosclerotic plaques, with no effective treatments currently available to halt this progression.
  • The study investigates the effects of Notoginsenoside R1 and protocatechuic aldehyde (R1-PCAD) on endothelial cells, revealing that this combination enhances nitric oxide production, improves endothelial function, and reduces inflammation and calcium deposition in a mouse model of atherosclerosis.
  • R1-PCAD works primarily through the NO-TGFβR1-YAP/TAZ signaling pathway, inhibiting key processes in vascular smooth muscle cells that lead to inflammation and calcification, thus presenting a potential new therapeutic strategy for vascular calcification.
View Article and Find Full Text PDF

Atherosclerosis and resulting cardiovascular disease are the leading causes of death in the US. Hyperhomocysteinemia (HHcy), or the accumulation of the intermediate amino acid homocysteine, is an independent risk factor for atherosclerosis, but the intricate biological processes mediating this effect remain elusive. Several factors regulate homocysteine levels, including the activity of several enzymes and adequate levels of their coenzymes, including pyridoxal phosphate (vitamin B6), folate (vitamin B9), and methylcobalamin (vitamin B12).

View Article and Find Full Text PDF

The role of glutathione peroxidase 4 (GPX4) in ferroptosis and various cancers is well-established; however, its specific contribution to colorectal cancer has been unclear. Surprisingly, in a genetic mouse model of colon tumors, the deletion of GPX4 specifically in colon epithelial cells increased tumor burden but decreased oxidized glutathione. Notably, this specific GPX4 deletion did not enhance susceptibility to dextran sodium sulfate (DSS)-induced colitis in mice with varied iron diets but showed vulnerability in mice with a vitamin E-deficient diet.

View Article and Find Full Text PDF

Natural Antioxidant-Based Nanodrug for Atherosclerosis Treatment.

Small

December 2023

College of Biomedical Engineering and National Engineering Research Center for Biomaterials, Sichuan University, 29 Wangjiang Road, Chengdu, 610064, China.

Natural antioxidants are always considered as candidates for the antioxidative therapy of atherosclerosis (AS) due to their good safety profile. However, restricted to their limited reactive oxygen species (ROS) elimination and rapid metabolism, the natural antioxidants' treatment suffers from the undesirable clinical outcomes. Herein, a new natural antioxidant-based nanodrug (VC@cLAVs) that can overcome above issues is developed to treat AS by loading natural antioxidant vitamin C (VC) into the natural antioxidant lipoic acid (LA)-constructed cross-linked vesicles.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!