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Abstract. Basophilic hypertrophic foci of the parotid glands characterized by focal hypertrophy and hyperchromasia of acinar cells was seen in Sprague-Dawley rats and Swiss mice with overall incidences of 4.8% (102/ 2,138) and 0.6% (4/723), respectively. In rats, the incidence increased significantly with age, but the size and number of the lesions per rat did not. Based on the similar incidence in both control and treated animals, lesions were considered to be spontaneous. Their morphology and growth pattern suggested that they were neither degenerative, necrotic, hyperplastic/preneoplastic, nor neoplastic, but, that they are a distinct pathologic entity of a nature not yet determined.In spite of the large number of rodents that have been examined histopathologically in recent years, reports of spontaneously occurring lesions of the parotid glands in laboratory rodents are relatively infrequent. The reasons may be that the salivary glands 1) have not been considered to be a major organ and have not been routinely examined histologically in the past, 2) have few primary lesions with low incidence, and 3) have rarely been shown to be a target organ in toxicity and oncogenicity studies.Focal changes of the parotid acinar cells characterized histomorphologically by enlargement and increased basophilia have been seen in rats and mice used in safety assessment tests of chemicals at Haskell Laboratory. Similar lesions have been reported to occur spontaneously or to be induced experimentally in several strains of rats.IJ1J2J5J6 However, the occurrence of such lesions in Sprague-Dawley rats and mice has not been documented. In addition, this lesion has not been described in humans. Generally, information regarding the nature, classification, terminology, and incidence of this lesion is fragmented and confusing. Because of its characteristic histomorphologic appearance, the lesion is called basophilic hypertrophic focus in this report. This paper reports the incidence and histomorphology of the lesion in rats and mice and discusses its nature, significance, and terminology. Materials and MethodsMale and female C r K D @ (SD)BR Sprague-Dawley rats and Crl:CD@ -1 (1CR)BR Swiss mice (Charles River Breeding Laboratories, Wilmington, MA or Kingston, NY) were used as untreated control or treated animals in recently conducted safety evaluation tests of chemicals by either feeding or inhalation exposures. Animals were separated by sex and housed either individually (mice only) or up to three in suspended stainless steel wire-mesh cages in light, humidity, and temperature-controlled rooms. PurinaB rodent chows [mixed with 1.0% (w/w) Mazola@ corn oil to the ground feed for feeding studies] and tap water were available ad libitum except during periods of inhalation exposure. Formalin-fixed, paraffin-embedded tissue sections were stained with hematoxylin and eosin and examined by light microscopy.To examine the effect of age, sex, and type of treatment (feeding versus inhalation, and untreated control versus treated) on the occurren...

Inhalation studies were conducted to determine the potential toxicity and/or potential neurotoxicity of cyclohexane. Groups of rats and mice were exposed to 0, 500, 2000, or 7000 ppm concentrations of cyclohexane vapor 6 hr/day, 5 days/week for 14 weeks. Subgroups of rats and mice were further observed during a 1-month recovery period. Functional observational battery (FOB) and motor activity (MA) behavioral tests were conducted on rats. These tests were conducted prior to the exposure series and during weeks 4, 8, and 13 on non-exposure days. Clinical pathology evaluations were conducted after approximately 7, 13, and 18 weeks. Approximately 14 and 18 weeks after study initiation, tissues from rats and mice were histologically processed and evaluated by light microscopy. During exposure to 2000 or 7000 ppm, rats and mice had a diminished response or an absent response to delivery of a punctate auditory alerting stimulus. Immediately following removal of rats from the inhalation chambers, 7000 ppm males and females and 2000 ppm females displayed a compound-related increase in the incidence of wet and/or stained fur (which occurred in the areas of the mouth, chin, and/or perineum). These signs were transient, were not observed during exposure or prior to exposure the following day, and were not associated with any behavioral or morphological changes. During exposure sessions, mice exposed to 7000 ppm exhibited clinical signs of toxicity which included hyperactivity, circling, jumping/hopping, excessive grooming, kicking of rear legs, standing on front legs, and occasional flipping behavior. Clinical signs of toxicity observed in 7000 ppm mice immediately after exposure included hyperactivity, hyperreactivity, ruffled fur (females only), gait abnormalities, spasms in both rear legs, and excessive grooming (males only). The clinical signs observed in mice during and immediately after exposure were transient, and were not present prior to the subsequent exposure. A few mice exposed to 2000 ppm appeared hyperactive during exposure in the latter portion of the study. There were no compound-related changes in mean body weights, body weight gains, food consumption, food efficiency, or mortality; and there were no ophthalmological abnormalities in rats or mice. In addition, there were no compound-related effects on 37 different behavioral parameters assessed during the FOB or during motor activity tests in rats. Male and female mice exposed to 7000 ppm had slight increases in measures of circulating erythrocyte mass (red blood cells, hemoglobin, hematocrit) and plasma protein concentration (males only). Male rats and male and female mice exposed to 7000 ppm had significantly increased relative liver weights, and 7000 ppm male mice also had significantly increased absolute liver weights at the end of the exposure period. At the end of the 1-month recovery period, absolute and relative liver weights of male and female mice were similar to control. However, relative liver weights of 7000 ppm male rats continued to be signifi...

An external ear lesion designated as auricular chondropathy in aging Crl:CD rats was reported. One hundred eighty (180) of 4,876 rats (3.7%) had ear deformity. Grossly, the ears were thickened, nodular, or disfigured. Both ears were affected in most rats. The lesions primarily involved the cartilaginous plate and were associated with two processes--chondrolysis and granulomatous inflammation. The detailed morphogenesis of the lesions is described, but the etiology of the lesions is unknown. Auricular chondropathy in rats and relapsing polychondritis in man are compared.