Abstract
It has already been reported that anaphylatoxin (AT) is closely related to inner ear lesions. In this study the pathology of inner ear damage caused by AT was investigated in Hartley strain and C4 deficient guinea pigs (C4D-GP). Although the biological activity of C3a and C5a is strong, it is of short duration, and the resulting ear damage is considered to be reversible. Because of the cellular degeneration caused by this slight damage, the damage owing to continuously activated C4a is thought to be irreversible, that is, atrophy in the stria vascularis, degeneration and sloughing of the cochlear neurons, and stretching of Reissner's membrane, and C4a is therefore considered to be requisite for the manifestation of inner ear damage.
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