Acrylamide disrupts elemental composition and water content of rat tibial nerve. II. Schwann cells and myelin

The effects of subchronic and subacute acrylamide (ACR) intoxication on elemental composition (Na, P, S, Cl, K, Ca, Mg) and water content of Schwann cell body cytoplasm and myelin were assessed in rat tibial nerve. Electron probe X-ray micro-analysis demonstrated that, in control rats, peripheral nerve glia and myelin exhibited highly characteristic distributions of elements and water and that ACR intoxication was associated with disruption of this normal subcellular distribution. When rats were intoxicated with ACR by either the oral (2.8 mm in drinking water for 15, 22, 30, and 60 days) or the intraperitoneal (50 mg/kg/day ×5 and 10 days) route, an exposure-dependent loss of cytoplasmic Na, K, P, Cl, Mg, and water regulation was detected in Schwann cell cytoplasm. Maximum development of elemental deregulation occurred after 30 days of oral ACR exposure and 10 days of ip treatment. The cytoplasmic elements involved and their corresponding quantitative changes were similar regardless of the route of ACR intoxication. Analysis of myelin revealed that both oral and parenteral ACR exposure caused early, persistent increases in dry weight Na, P, and water content. However, Cl dry weight concentrations were increased by oral exposure and decreased by ip ACR injection. Results of this study indicate that ACR intoxication is associated with a significant disturbance of subcellular element and water distribution in tibial nerve Schwann cells and myelin. The pattern of elemental disruption is typical of reversible cell damage and, therefore, Schwann cell injury might play a role in the expression of ACR neurotoxicity.