Cytoskeletal components, especially
f-actin (filamentous actin), are responsible for neurite extension and maintenance. Alterations in neurite length and quality precede in vitro cell death induced by organophosphorus (OP) compounds and implicate
f-actin proteins in this process. We, therefore, investigated changes in
f-actin in SH-SY5Y human
neuroblastoma cells exposed to 0.1 and 1 mM
paraoxon,
parathion,
phenyl saligenin phosphate (PSP), tri-ortho-tolyl
phosphate (
TOTP),
triphenyl phosphite (TPPi), and di-isopropyl phosphorofluoridate (
DFP) for 0-48 h. The
f-actin was measured by flow cytometry in cells labeled with Alexa 488
phalloidin. The relative amount off-actin was compared to total
protein levels as determined by spectrophotometry. The cellular content of
f-actin significantly decreasedfollowing exposure to PSP (0.1 mM, >30 min; 1 mM, >15 min),
TOTP (0.1 mM, 16 h; 1 mM, >15 min), TPPi (1 mM, >4 h),
paraoxon (1 mM, >24 h), and
parathion (1 mM, 48 h). Exposure to
DFP (0.1 and 1 mM) did not significantly alter
f-actin content at any time point. Exposure to
parathion (0.1 mM, 48 h) significantly increased the amount of cellular
f-actin. Total
protein was significantly decreased after exposure to PSP (0.1 and 1 mM, >8 h) and TPPi (1 mM, 48 h). Significant increases in total
protein were observed following exposure to
parathion (0.1 mM, >3 h). Consistent alterations in the
protein content of
DFP-exposed samples were not observed. These results suggest that the loss off-actin is an early event following OP compound exposure and that this loss significantly precedes a loss of
protein content for some OP compounds (PSP, TPPi). Results also imply that under other exposure conditions (
TOTP,
paraoxon,
parathion) alterations in the
f-actin content are independent of
protein content.