Qualitative and quantitative ultrastructural studies were performed on mitochondria of leukemic monoblasts from 15 patients with acute monoblastic leukemia. Similar comparative observations were made on mitochondria of myeloblasts from 14 hematologically normal controls. No significant quantitative differences were noted between normal and leukemic mitochondria. Area measurements were approximately equal. Qualitative differences between the two groups consisted of increased numbers of irregularly shaped mitochondria, damaged mitochondrial membranes, mitochondria with damaged matrix, and small granules in mitochondria in the leukemic group. Leukemic cells exhibited nuclear-mitochondrial contact and virus-like particles within damaged mitochondria. To confirm the presence of virus-like particles and to aid in our understanding of nuclear-mitochondrial interaction, a C-type virus producer MSV-MLV infected rat embryo cell culture was used for additional analysis. Mitochondrial abnormalities and increased frequency of virus in damaged mitochondria, often attached to mitochondrial membranes, were noted. Several lysosomes exhibited accumulations of virus and budding into lysosomes from lysosomal membranes. Mitochondria are important organelles in glycolytic-oxidative phosphorylation pathways, and carry extranuclear genetic information. Further studies of morphologic and biochemical abnormalities of leukemic mitochondria and the interaction between the mitochondria and the nuclei in leukemic cells are needed to provide researchers with data on extranuclear factors operating in oncogenesis.
Cardiac minute volume, renal blood flow, pulse volume, heart rate and urinary output were determined by means of experiments made on 10 mongrel dogs. Anaesthesia was maintained by nitrous oxide/oxygen mixture administered with Ketamine. Under the conditions described it was observed that -- contrary to what is found in human patients -- cardiac and renal minute volume as well as pulse volume are significantly decreased. No significant changes has been observed in the heart rate. Whilst urinary output was decreased, the excretion of individual electrolytes was found to be different.
Acid phosphatase isozymes were investigated in cancerous prostatic tissue (4 cases) and benign prostatic hyperplasia (6 cases). Electron-microscopic histochemical examination of cancer tissue revealed irregular acid beta-glycerophosphatase staining in various cell organelles, including the plasma membrane, which was not seen in non-malignant tissue. Cancerous tissue homogenates also contained isozymic acid phosphatase species with high electrophoretic mobility, which was not detectable in benign tissue unless treated with detergent. Fractionation by differential centrifugation confirmed that much of the acid phosphatase activity in cancer tissue was extra-lysosomal. The detection of these isozyme properties may provide an opportunity, by means of tissue investigations, to define tumour stages earlier than on the basis of increased levels of serum acid phosphatase activity indicative of stage IV (D) prostatic cancer.
The various acid phosphatase isozymes can be distinguished on the basis of their biochemical properties or their net electrical charge. Four main groups of isozymes hydrolyze β-glycerophosphate: the fastest-moving form seemed to be related to the cancerous state. The quantity of enzyme, either in the whole homogenate or in cytoplasmic fractions was not a useful criteria for cancer, however, while the distribution of acid phosphatase in subcellular structures was characteristic in cancer cases. Cell fractions were obtained by differential centrifugation, but were contaminated with prostatic secretions.
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