Metabolism of benzo(a)pyrene by multinucleated giant cells.
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Animals↗
Biomedical subjects
O Black
Publications and source records attributed to O Black.
Origin of tubular complexes developing during induction of pancreatic adenocarcinoma by 7,12-dimethylbenz(a)anthracene.
Implantation of 7,12-dimethylbenz(a)anthracene (DMBA) into the pancreas of rats has been shown to induce adenocarcinoma. Complexes of tubules, which have the appearance of proliferated intralobular ducts, frequently appear during tumor development. These complexes were studied by light and electron microscopy to determine their method of formation. In addition, a tubular complex was reconstructed from serial sections to determine its three-dimensional configuration. Although tubular complexes have been thought by others to result from ductal proliferation, the following observation indicate that they originate from zymogen-granule-containing cells: a) there is a continuum of transitional stages between acini and tubules, b) most tubules decrease in size and are replaced by connective tissue (evidence of regression rather than proliferation), c) few mitotic figures are seen in tubular complexes, d) the tubules comprise many cells which have an abundance of rough endoplasmic reticulum, an organelle which is sparce in ducts, and e) the three-dimensional arrangement of tubules appears identical to the branching, anastomosing arrangement of zymogen-granule-containing cells of the normal rat pancreas. Control animals in which only sutures were placed in the pancreas showed minimal reaction. It is concluded that "acini" become recognized as tubules when loss of zymogen granules accompanies tumor induction by DMBA. Transformation of these cells could be erroneously interpreted as transformation from proliferating ducts.
9,10-Dimethyl-1,2-benzanthracene↗
Histofluorescence of 3-methylcholanthrene metabolites in the rat pancreas.
Pancreases of Long-Evans rats were treated in vitro and in vivo with 3-methylcholanthrene and examined by histofluorescence techniques. For in vitro studies, tissue sections were dipped in 3-methylcholanthrene and incubated in vitro. These sections revealed that acinar and ductal epithelium had equal fluorescence which suggested equal metabolic capability. For in vivo experiments, 3-methylcholanthrene was injected intraperitoneally and the rats were killed 60 min later. Two additional rats were provided with biliary cannulae to divert bile from the pancreatobiliary ducts. Frozen sections, 16 mu in thickness, were prepared and examined under the fluorescence microscope. The sections revealed that fluorescence was concentrated in the epithelium and lumen of ducts. Animals with diversion of bile from the pancreatobiliary ducts had similar intensity and distribution of fluorescence. The in vivo studies showed that ductal epithelium was exposed to greater concentrations of carcinogen than nonductal epithelium. These observations provide a link between epidemiological studies that show an increased incidence of pancreatic adenocarcinoma in populations exposed to environmental carcinogens and morphological studies that show the ductal cell to be the most likely cell of origin.
Animals↗
Pancreatic acinar cell metabolism and function.
This review outlines progress made during the past 11 years in research related to pancreatic acinar cell metabolism and function. We have reviewed information gained at the cellular level concerning structural and functional relationships, and effects of fasting and feeding, as well as the action of gastrointestinal hormones and cholinergic agonists on acinar cells. In toto, this information outlines a significant role for gastrointestinal hormones as mediators of secretion, synthesis, and control of trophism. This information provides a basis for more sophisticated inquiries as to the mechanisms of injury of alcohol and drugs. The information may prove helpful in developing diagnostic modalities for pancreatic disease, as well as understanding the processes involved in neoplastic transformation.
Amino Acids↗
Fine structure of pancreatic adenocarcinoma induced in rats by 7,12-dimethylbenz(a)anthracene.
We induced pancreatic adenocarcinomas in Long-Evans rats by placing crystals, 2-3 mg, of 7,12-dimethylbenz[a]anthracene (DMBA) in a 2- to 3-mm incision in the "head" of the pancreas approximately 1 cm from the duodenum. The incisions were closed with one or two silk sutures. The animals were killed 4-10 months after DMBA implantation, and nodules were removed and routinely prepared for light and/or electron microscopic study. Histologic organization varied from normal, through areas of tubule-like structures, to sheets of pleomorphic tumor cells. Electron microscopic study of tumor cells revealed large electron-lucent nuclei that frequently had irregular outlines and prominent nucleoli. The predominant feature of the cytoplasm was abundant rough endoplasmic reticulum. Zymogen granules were rare. Adjacent cells sometimes were jointed by an apical junctional complex to form a lumen into which projected irregular microvilli. A basal lamina sometimes occurred at the bases of the tumor cells. The fine structural similarity of these tumor cells to acinar cells was noted.
9,10-Dimethyl-1,2-benzanthracene↗
Experimental induction of pancreatic adenocarcinoma in rats.
Adenocarcinomas of the pancreas were experimentally induced in rats after the implantation of 7,12-dimethylbenz[alpha]anthracene (DMBA). Rats were anesthetized with Nembutal, the pancreas was exposed, and a 2- to 3-mm incision was made in the "head" of the pancreas approximately 1 cm from the duodenum. Crystalline DMBA (2-3 mg) was implanted and the incision was closed with silk suture. Eight % of animals developed tumors in the pancreas from 119 to 363 days after implantation (mean, 194 days). Ten animals developed tumors in less than 180 days. The adenocarcinomas were invasive, metastasized, and had pronounced ductal cell characteristics. The light-microscopic morphology of these pancreatic tumors was presented.
9,10-Dimethyl-1,2-benzanthracene↗