LECTIN-BINDING PATTERN OF SCHWANN-CELLS AND MACROPHAGES IN 2,5-HEXANEDIONE-INDUCED AXONAL DEGENERATION IN RATS

Citation
Mr. Carratu et al., LECTIN-BINDING PATTERN OF SCHWANN-CELLS AND MACROPHAGES IN 2,5-HEXANEDIONE-INDUCED AXONAL DEGENERATION IN RATS, Archives of toxicology, 69(3), 1995, pp. 160-164
Citations number
25
Categorie Soggetti
Toxicology
Journal title
ISSN journal
03405761
Volume
69
Issue
3
Year of publication
1995
Pages
160 - 164
Database
ISI
SICI code
0340-5761(1995)69:3<160:LPOSAM>2.0.ZU;2-0
Abstract
The lectin binding pattern of both Schwann cells and macrophages has b een studied during axonal degeneration induced in the rat sciatic nerv e by chronic administration of 2,5-hexanedione (0.8 ml/kg per day i.p. for 20 days). In particular, the present study aimed to establish a p ossible relationship between macrophage activation and expression of l ectin binding sites. To identify and distinguish between Schwann cells and macrophages, electron microscopy was combined with the lectin sta ining method. On 2,5-hexanedione injury, a drastic disorganization of both axon and myelin sheath occurred and nerve fibers were replaced by a chain of ovoids. Besides the well-established concept that Schwann cells and macrophages cooperate in the removal of the myelin debris du ring axonal degeneration, evidence is presented that expression of bin ding sites to lectins is closely related to macrophage activation. Mon ocytes occasionally present in control nerves were labelled only by Co n A and sialidase-peanut sequence; in 2,5-hexanedione degeneration mon ocytes, prephagocytes (macrophages with minute bubbles) and phagocytes (macrophages with large bubbles) were labelled also by peanut, wheat germ and BSA I-B-4; moreover, phagocytes were labelled by soybean as w ell, thus showing a clearly differentiation-dependent binding pattern. Since changes in lectin binding pattern may reflect changes in comple x carbohydrate structures, the results show that the expression of cer tain glycoproteins may be closely related to activation of macrophages in response to toxic injuries.