The effects of acute phase phosphoplipids from patients with chronic fatigue syndrome on the sodium channel in tissue culture

Abstract

Acute phase phospholipids isolated from the sera of patients with clinically diagnosed chronic fatigue syndrome (CFS) were examined for effects on the sodium channel of mouse neuroblastoma cells in tissue culture after studies suggested a structural correlation between CFS lipids and the lipophilic marine toxin, ciguatoxin. The neuroblastoma cell bioassay is a directed cytotoxicity assay that records sensitive changes in the sodium channel of neuroblastoma cells in the presence of sodium channel activators or inhibitors. The ciguatoxins are characterized by their ability to cause the persistent activation of voltage‐sensitive sodium channels, leading to increased cell Na+ permeability. Ciguatera fish poisoning in humans is characterized by neurological, gastrointestinal, and cardiovascular manifestations that are similar to the symptoms of CFS.Several lipids were examined for sodium channel activity: ciguatoxin, cholesterol, cholesterol myristate, and the phospholipids isolated from CFS patients as well as antagonists gluconate, ursodeoxycholic acid, d‐ribose, and anti‐CTX antibody. Results indicate that cholesterol and cholesterol myristate have weak but observable interactions at the sodium channel as activators, and that CTX and CFS lipids both have strong activity as sodium channel activators. However, studies revealed that none of the potential antagonists evaluated were effective at blocking the activity of the lipids at the sodium channel.[Supported in part by National CFIDS Foundation, and the Hokama‐Yagawa Fund]