MESANGIAL DISPOSAL OF GLOMERULAR IMMUNE DEPOSITS IN ACUTE MALARIAL GLOMERULONEPHRITIS OF RATS

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  • 1 January 1982
    • journal article
    • research article
    • Vol. 46  (2) , 209-214
Abstract
P-Bromophenylacetylurea (BPAU) is a neurotoxin known to cause intraaxonal accumulations of tubulovesicular materials and distal axonal degeneration. Two aspects of the pathology were studied in the peripheral nerves in rats: the comparative pathology of acute and chronic intoxication, and the ability of intoxicated neurons to regenerate. The rats were divided into acute and chronic intoxication groups. Rats acutely intoxicated received 1 i.p. injection (400 mg/kg) and developed paraparesis after 2 wk. Rats chronically intoxicated were given daily i.p. injections (10 mg/kg) for 2-7 mo. and paraparesis appeared after 8 wk. Both groups showed degeneration of distal nerves. By 3 wk rats in the acute intoxication group showed an 18-50% loss of axons in the distal phrenic nerve. Axons contained membranous trabeculae (tubules and vesicles); at later times, the tubulovesicular profiles increased and, subsequently, axons degenerated. In these animals, regenerating sprouts were first seen 3 wk after stopping BPAU; these sprouts also contained tubulomembranous structures which persisted for 18 mo. After 2-3 mo., the chronic intoxication group showed a reduction in the number of axons in the distal phrenic nerve. Surving axons showed tubulovesicular profiles similar to those observed in acutely intoxicated rats. In this group of rats, axonal regeneration was also characterized by the presence of membranous profiles in the axonal sprouts. Observations indicate that the pathologic changes caused by BPAU are independent of the rate of administration of the drug. The long-standing abnormalities in the regenerating sprouts suggest a persistent toxic effect on axons. Since membranes are delivered and retrieved through fast anterograde and retrograde transport, the accumulation of membranes may be related to abnormalities in these systems. BPAU appears to be a useful agent to study the pathogenetic mechanisms causing tubulovesicular neuropathies.