Hepatic nuclear and cytoplasmic effects following intermittent feeding of rats with di(2-ethylhexyl) phthalate

The effects on rats of intermittent feeding with the peroxisome proliferator and hepatocarcinogen di(2-ethylhexyl) phthalate (DEHP) have been examined. Male Wistar rats were fed for alternate 7-day periods diets containing 20,000 ppm DEHP or the control diet. The rats were examined 3 days after the start or recommencement of administration of the DEHP-containing diet or after 7 days on the control diet. After the commencement or recommencement of feeding with DEHP the expected increases in liver weight and in the number of peroxisomes were found. The increase in liver: body-weight ratio in response to administration of DEHP-containing diets was greater in rats that had been previously exposed to the compound, but re-administration of DEHP had a less marked effect on the increase in peroxisome number. Morphometric analysis showed that administration of DEHP-containing diets resulted in an increase in cell number in the liver and that a fall in the cell number occurred after the rats had been returned to the control diet for 7 days. Analysis of nuclear size gave results consistent with an increase in tetraploid hepatocytes after treatment with DEHP which was reversed when the rats were returned to control diet.     

Quantification of tissue plasma volume in the rat by contrast-enhanced magnetic resonance imaging

Magnetic resonance imaging enhanced with a macromolecular contrast medium (MMCM), albumin-Gd-DTPA, was used to estimate the plasma volume in vivo in the myocardium, lung, liver, and skeletal muscle of 10 normal rats. The plasma volumes of the same tissues in a parallel group of six rats were estimated in vitro by a conventional radioisotopic technique (¹¹¹In-transferrin). Plasma volumes of myocardium, lung, liver, and skeletal muscle estimated by the MR technique (μl plas. ia cc-¹ of tissue) were 101,109,163, and 11.0, respectively, while plasma volumes measured by the In-transferrin radioisotope technique (mg plasma g-¹ of tissue) were 78.6, 215,143, and 11-2, respectively. Assuming a ratio of densities of aerated lung to blood of 0.45 and of other tissues to blood of 1.0, correlation between the methods was excellent (R² = 0.99) indicating that MR imaging enhanced with MMCM permits reliable in vivo estimation of tissue plasma volume in the rat.     

An autoradiographic study of periodontal development in the mouse

Tritiated thymidine was injected into 10- and 13-day-old mice because at this age the third molar is at the appropriate stage of development. At set intervals, the mice were killed and the distribution of labeled cells within the dental papilla and follicle examined. The change in labeling index with time was measured for defined areas in the papilla and follicle. It was shown that, during the late bell stage of development, cells moved from the papilla into the follicle. It was concluded that the pulp, rather than the investing layer of the follicle, is the source of the periodontium and that growth of the pulp and periodontal tissues could generate an important force contributing to tooth eruption.     

Putative glutamatergic and/or aspartatergic cells in the main and accessory olfactory bulbs of the rat

The "transmitter-specific" retrograde axonal tracer 3H-D-aspartate has been used to demonstrate neurons in the olfactory bulb which putatively utilize aspartate and/or glutamate as their neurotransmitter and which send an axon either to the piriform cortex or within the bulb itself. Injections of 3H-D-aspartate into layer I of the anterior piriform cortex, in the zone of termination of axons from the olfactory bulb, labeled only a few cells in the main olfactory bulb, located in the mitral and external plexiform layers. Although these cells resembled mitral and tufted cells, they tended to have smaller somata than other mitral or tufted cells and apparently form a distinct subpopulation of relay cells. In contrast, many of the mitral cells of the accessory olfactory bulb were labeled by the same injections of 3H-D-aspartate, probably as a result of involvement of the accessory olfactory tract or its bed nucleus in the injection site. Similar injections of the "nonspecific" tracer HRP into the anterior piriform cortex labeled most of the cells in the mitral cell layer of both the main and accessory olfactory bulbs, and some tufted cells in the external plexiform layer. It is concluded that only a small, distinct subpopulation of the mitral or tufted cells of the main olfactory bulb are aspartatergic and/or glutamatergic, while many (at least) of the mitral cells of the accessory olfactory bulb use the excitatory amino acids as transmitters. Injections of 3H-D-aspartate directly into the main olfactory bulb also failed to label the mitral and deeply situated tufted cells. However, a few cells were labeled in the periglomerular region, the superficial external plexiform layer, and the granule cell layer near the injection site. These labeled cells were smaller than mitral and tufted cells but generally larger than periglomerular or granule cells. They may represent a population of glutamatergic or aspartatergic short axon cells. In addition, small cells of an unknown type were labeled in the olfactory nerve layer following injections in the deepest part of the bulb. These cells do not correspond to any of the well characterized cell types of the olfactory bulb.