ABSTRACT
Dietary administration of the whole spice turmeric (0.2%, 1.0%, 5.0%) or ethanolic turmeric extract (ETE, 0.05%, 0.25%) for 14 days, at doses reported to be cancer preventive in model systems, were found to be hepatotoxic in mice. Histopathological evaluation showed coagulative necrosis accompanied by a zone of regenerating parenchymal cells of liver. The ultrastructural changes in liver parenchymal cells were non-specific reaction to injury. Results suggest mouse to be a susceptible species for turmeric induced toxicity.
Subject(s)
Administration, Oral , Animals , Condiments/adverse effects , Curcuma , Female , Chemical and Drug Induced Liver Injury/etiology , Mice , Microscopy, Electron , Plant Extracts/adverse effectsABSTRACT
Clinical evaluation, upper gastrointestinal endoscopy and electron microscopy of mucosal biopsies from antrum, body and fundus of stomach were performed in three control subjects and 17 habitual tobacco chewers. Electron microscopic abnormalities such as discontinuous, fragmented basement membrane with reduction in hemidesmosomes, and widened intercellular spaces filled with clusters of desmosomes were found in the gastric mucosa of habitual tobacco chewers; these were similar to those reported in experimental carcinogenesis and leukoplakia. It is concluded that habitual chewing of tobacco produces electron microscopic alterations in the human gastric mucosa which may be important precursors for gastric malignancy.
Subject(s)
Adult , Gastric Mucosa/ultrastructure , Humans , Microscopy, Electron , Plants, Toxic , Tobacco, SmokelessABSTRACT
Seventeen chronic tobacco chewers and three control subjects underwent clinical evaluation, upper gastrointestinal endoscopy and esophageal mucosal biopsies. The esophageal biopsies were processed and examined under the electron microscope. A large number of ultrastructural abnormalities such as discontinuous, fragmented basement membrane, with reduction in hemidesmosomes, widened intercellular spaces were found in the esophageal mucosa of chronic tobacco chewers which resembled the ultrastructural features of experimental carcinogenesis and leukoplakia. It is concluded that chronic chewing of tobacco produces ultrastructural abnormalities in the esophageal mucosa which could be important precursors for esophageal malignancy.
Subject(s)
Basement Membrane/ultrastructure , Biopsy , Epithelium/ultrastructure , Esophagus/ultrastructure , Humans , Intercellular Junctions/ultrastructure , Microscopy, Electron , Mucous Membrane/ultrastructure , Plants, Toxic , Time Factors , Tobacco, Smokeless/adverse effectsABSTRACT
In this study initially a precancerous condition, leukoplakia, was develop at 6 weeks treatment of DMBA whereas in the animals treated both DMBA + Vit. A, leukoplakia was seen at 10 weeks followed by papilloma or nodules at 12 weeks. Tumours induced by DMBA were more in number than DMBA + Vit. A treated tumours. The histological and ultrastructural changes were enhanced and prominent in DMBA treated animals at 12 weeks, where as these changes were considerably less in animals treated with DMBA + vit. A at 12 weeks.
Subject(s)
9,10-Dimethyl-1,2-benzanthracene/toxicity , Animals , Cricetinae , Female , Leukoplakia, Oral/chemically induced , Male , Mesocricetus , Microscopy, Electron , Mouth Neoplasms/chemically induced , Papilloma/chemically induced , Vitamin A/pharmacologyABSTRACT
The utility of hamster cheek pouch model for studies on oral carcinogenesis has been explored using 9,10-dimethyl-1-2-benzanthracene as a carcinogen. Based on the morphological, histopathological and electron microscopic observations the hamster cheek pouch carcinogenesis can be separated into different stages starting from the normal to the fully grown carcinomas. This system is reliable, precise, consistent and can be used for the evaluation of different agents for initiating or promoting effects and as well as for the studies on mechanism of oral carcinogenesis.