Rm. Lopachin et al., EFFECTS OF ACRYLAMIDE ON SUBCELLULAR-DISTRIBUTION OF ELEMENTS IN RAT SCIATIC-NERVE MYELINATED AXONS AND SCHWANN-CELLS, Brain research, 608(2), 1993, pp. 238-246
Electron probe X-ray microanalysis was used to determine whether exper
imental acrylamide (ACR) neuropathy involves deregulation of subcellul
ar elements (Na, P, S, Cl, K, Ca and Mg) and water in Schwann cells an
d small, medium and large diameter myelinated axons of rat sciatic ner
ve. Results show that in proximal but not distal sciatic nerve, ACR tr
eatment (2.8 mM in drinking water) was associated with an early (15 da
ys of exposure), moderate increase in mean axoplasmic K concentrations
(mmol/kg) of medium and small diameter fibers. However, all axons in
proximal and distal nerve regions displayed small increases in dry and
wet weight contents of axoplasmic Na and P. As ACR treatment progress
ed (up to 60 days of exposure), Na and P changes persisted whereas pro
ximal axonal K levels returned to control values or below. Alterations
in mitochondrial elemental content paralleled those occurring in axop
lasm. Schwann cells in distal sciatic nerve exhibited a progressive lo
ss of K, Mg and P and an increase in Na, Cl and Ca. Proximal glia disp
layed less extensive elemental modifications. Elemental changes observ
ed in axons are not typical of those associated with cell injury and m
ight reflect compensatory or secondary responses. In contrast, distal
Schwann cell alterations are consistent with injury, but whether these
changes represent primary or secondary mechanisms remains to be deter
mined.