Re. Cohen et al., INDUCTION OF TYPE-2 CYSTATIN IN RAT SUBMANDIBULAR GLANDS BY SYSTEMICALLY ADMINISTERED AGENTS, Archives of oral biology, 38(4), 1993, pp. 319-325
An inducible type 2 cystatin has earlier been characterized in submand
ibular glands and kidneys of rats treated with isoproterenol, as well
as in kidneys of rats with experimental renal disease. The purpose now
was to determine whether giving agents that have systemic toxicity co
uld also be associated with induction of cystatin in rat salivary glan
ds. Female Wistar rats (200-250 g) were given isoproterenol, cyclocyti
dine, potassium dichromate or turpentine oil. After autopsy, the organ
s were sectioned, fixed in 10% formalin, and processed routinely. Para
ffin sections were processed for both the peroxidase-antiperoxidase an
d the avidin-biotin-alkaline phosphatase immunocytochemical methods. T
he submandibular glands of rats given cyclocytidine had generalized, s
trong staining of acinar cells, as well as occasional weak staining wi
thin granular convoluted tubules. Animals given either potassium dichr
omate or turpentine oil exhibited moderate staining for cystatin in su
bmandibular acini. Rats given isoproterenol as a positive control exhi
bited strong acinar staining throughout the submandibular gland, while
the glands of untreated rats were unreactive. Inducible type 2 cystat
in could not be detected in the parotid or sublingual glands, or in tr
achea, lung, stomach, small intestine, large intestine, spleen, liver
and pancreas, after treatment with any of the systemic agents evaluate
d. The results indicate that elaboration of type 2 cystatin can be ind
uced by a variety of systemically administered agents other than isopr
oterenol, and suggest that elaboration of type 2 cystatin may represen
t a more generalized response to tissue injury.