Female Fischer 344 (F344)/N rats (10 per exposure group) were exposed to 2-butoxyethanol (BE) vapors (0, 31, 62.5, 125, 250, or 500 ppm 6 h/d, 5 d/wk, for 13 weeks) to characterize its prechronic toxicity. Dental lesions consisting of bilateral multifocal dental pulp thrombosis, pulp infarction, and odontoblast infarction were noted in the maxillary incisors of 3 of 4 rats from the 500-ppm group that were sacrificed when moribund during the first week of exposure. In addition, 1 rat from the 500-ppm group that was sacrificed on day 32 had similar unilateral incisor lesions but with additional findings consistent with a unilateral maxillary incisor fracture. In contrast, rats sacrificed after 13 weeks of exposure lacked dental lesions. In conclusion, BE has the potential to cause pulp thrombosis and odontoblast infarction in female rats. The apparent variability in response to BE noted in moribund sacrificed vs terminally sacrificed rats was attributed to development of tolerance to BE-induced hemolysis and subsequent incisor regeneration.

Administration, Inhalation↗

PubMedDate not supplied

Atypical tubule hyperplasia and renal tubule tumors in conventional rats on 90-day toxicity studies.

Bilateral, multicentric renal tubule tumors were found in 4 rats at the termination of 3 separate 90-day toxicity studies during the safety evaluation of 3 unrelated chemicals. The 3 studies were conducted at 2 separate locations, but the rats used were obtained from the same commercial source. The rat strains were Fischer-344 (1 male and 1 female case) and Sprague-Dawley (2 female cases). Three of the renal tumor cases were from either the high-dose or mid-dose treatment groups, and 1 case was an untreated control. The tumors were accompanied by multiple foci of atypical tubule hyperplasia but only in the tumor-bearing rats. There were no lesions associated with renal tumor pathogenesis in any of the remaining treated or untreated animals in the 3 studies. In addition, there was no indication of nephrotoxicity in the treated or untreated animals. Tumor morphology was characterized by a generally vacuolated appearance, eosinophilia, cytoplasmic and nuclear pleomorphism, and conspicuously hypertrophied nucleoli. The renal tubule tumors in these 90-day studies were compared to hereditary renal tubule tumors occurring in the Eker rat, a Long-Evans derivative with a genetic predisposition to this tumor type. The multiplicity of renal tubule tumors, early age of onset, and tumor morphology described in the cases from the 90-day studies were very similar to those characterizing the hereditary renal tumor model.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

PubMedDate not supplied

Disseminated thrombosis and bone infarction in female rats following inhalation exposure to 2-butoxyethanol.

Groups of 10 male and 10 female F344/N rats were exposed to 0, 31, 62.5, 125, 250, and 500 ppm of 2-butoxyethanol (BE) by inhalation, 6 hr/day, 5 days/wk, for 13 wk. Four moribund female rats from the 500 ppm group were sacrificed during the first 4 days of exposure, and 1 moribund female from the same group was sacrificed during week 5. Dark irregular mottling and/or loss of the distal tail were noted in sacrificed moribund rats. Similar gross lesions were noted in the terminally sacrificed females exposed to 500 ppm BE. Histologic changes noted in the day 4 sacrificed moribund rats included disseminated thrombosis involving the coccygeal vertebrae, cardiac atrium, lungs, liver, pulp of the incisor teeth, and the submucosa of the anterior section of the nasal cavity. Alterations noted in coccygeal vertebrae from the 500 ppm sacrificed moribund rats included ischemic necrosis and/or degeneration of bone marrow cells, bone-lining cells, osteocytes (within cortical and trabecular bone), and chondrocytes (both articular and growth plate), changes that are consistent with an infarction process. The moribund female rat that was sacrificed during week 5 and those female rats treated with 500 ppm and sacrificed following 13 wk of treatment lacked thrombi, but they had coccygeal vertebral changes consistent with prior infarction and transient or complete bone growth arrest. No bone lesions or thrombi were noted in the male rats treated with the same doses of BE. In conclusion, exposure to 500 ppm BE vapors caused acute disseminated thrombosis and bone infarction in female rats. Possible pathogenic mechanisms are discussed.

Administration, Inhalation↗

PubMedDate not supplied

A simple procedure for preparing and staining undecalcified sections of avian growth plate and metaphysis.

This report describes an inexpensive, rapid technique for preparing 4-micron-thick undecalcified sections of avian growth plate and metaphysis using paraffin embedment, rotary microtomes, and disposable knives. Sections were stained by von Kossa's technique with a hematoxylin-and-eosin counterstain.

Animals↗

PubMedDate not supplied

Experimental rickets in broilers: gross, microscopic, and radiographic lesions. II. Calcium deficiency.

Day-old broiler chicks were fed a calcium-deficient diet for 30 days. Gross, microscopic, and radiographic examinations of the proximal tibiotarsus were done at 2, 3, and 4 weeks of age. In 2-week-old chicks, the growth-plate proliferating-prehypertrophied zone (P-PHZ) was variably lengthened and disorganized, cartilage columns of the degenerating hypertrophied zone and metaphyseal primary spongiosa were shortened, and bone spicules of the secondary spongiosa were bordered by increased osteoid. In 3-week-old chicks, lesions were either similar or more pronounced, with the additional finding of metaphyseal peritrabecular fibrosis. In 4-week-old chicks, the P-PHZ decreased in relative length, osteoid seams and fibrous connective tissue were less prominent, and tibial dyschondroplasia-like lesions were present. Results demonstrated that dietary calcium deficiency produced rachitic lesions, that the lesions were very different from those of phosphorus deficiency or calcium excess, and that the lesions were variable over time.

Aging↗

PubMedDate not supplied

Experimental rickets in broilers: gross, microscopic, and radiographic lesions. III. Vitamin D deficiency.

Day-old broiler chicks were fed a vitamin D-deficient diet for 30 days. Gross, microscopic, and radiographic examinations of the proximal tibiotarsus were done at 2, 3, and 4 weeks of age. In 2-week-old chicks, there was variable lengthening and disorganization of the proliferating-prehypertrophied zone (P-PHZ), resorption of cartilage spicules in the degenerating hypertrophied zone and primary spongiosa, and lengthening of bone spicules in the secondary spongiosa; many bone surfaces were lined with increased osteoid. In 3-week-old chicks, there was a tendency for the P-PHZ to decrease in relative length and for cartilage spicules to increase in length. In 4-week-old chicks, however, there was marked lengthening of the P-PHZ, resorption of cartilage spicules, and replacement of the metaphysis with irregularly oriented islands of woven bone, osteoid, and loose fibrous connective tissue.

Aging↗

PubMedDate not supplied

Experimental rickets in broilers: gross, microscopic, and radiographic lesions. I. Phosphorus deficiency and calcium excess.

Day-old broiler chicks were fed diets high in calcium or low in phosphorus for 30 days. Chicks in both groups had similar gross, microscopic, and radiographic lesions. At 2 weeks, the growth-plate degenerating hypertrophied zone (DHZ) and metaphyseal primary spongiosa were lengthened and decreased in radiopacity. Metaphyseal vessels extended to the growth-plate hypertrophied zone (HZ), and osteoid seams were widened. At 3 and 4 weeks, lesions were similar; however, folding fractures were common and cartilage columns of the metaphysis were thinned and replaced with increased woven bone.

Animals↗