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The activities of inorganic pyrophosphatase, thymidine kinase and thymidine phosphorylase were measured in Ter-mutants of E. coli K12 which have a higher or a lower dTTP pool than the parent strain. The levels of inorganic pyrophosphatase and thymidine kinase were changed in the same direction and that of thymidine phosphorylase in the opposite direction in these mutants. [ABSTRACT FROM AUTHOR]

Mitochondria of osteosarcoma cells (143B) in culture have variable morphologies, classified according to the shape and size of the organelle as reticular, fragmented or intermediate. Synchronization and release from G0 has shown that the morphology of mitochondria oscillates between the reticular and fragmented state in a cell cycle dependent manner. Cells in G1 have reticular mitochondria while those in S phase have fragmented mitochondria. By using a novel method of fluorescence in situ hybridization, the morphology of mitochondria was correlated with mitochondrial DNA distribution. MtDNA molecules were seen in clusters of two to four along mitochondrial filaments. In the fully fragmented state, each mitochondrion contained at least one cluster. We discuss the importance of fission and fusion events in regulating the morphology of mitochondria, segregation of mtDNA and maintenance of the organelle's functional unity.

Complex I defects are one of the most frequent causes of mitochondrial respiratory chain disorders. Therefore, it is important to find new approaches for detecting and characterizing Complex I deficiencies. In this paper, we introduce a new set of monoclonal antibodies that react with 39-, 30-, 20-, 18-, 15-, and 8-kDa subunits of Complex I. These antibodies are shown to aid in diagnosis of Complex I deficiencies and add understanding to the genotype-phenotype relationships of different mutations. A total of 11 different patients were examined. Four patients had undefined Complex I defects, whereas the other patients had defects in NDUFV1, NDUFS2 (two patients), NDUFS4 (two patients), NDUFS7, and NDUFS8. We show here that Western blotting with these antibodies, particularly when used in conjunction with sucrose gradient studies and enzymatic activity measurements, helps distinguish catalytic versus assembly defects and further distinguishes between mutations in different subunits. Furthermore, different mutations in the same gene are shown to give very similar subunit profiles, and we show that one of the patients is a good candidate for having a defect in a Complex I assembly factor.

This study indicates 1. that there is an excess morbidity from lung cancer in miners, 2. that nonsmokers are overrepresented among lung cancer cases, and 3. that the induction time for lung cancer is about 10 years shorter in smokers.

The effect on lung function of exposure in an asbestos cement plant was investigated in male workers, employed more than 10 years. The exposed group was selected to exclude subjects with pneumoconioses and ex-smokers and consisted of 77 smokers and 48 never-smokers. Referents were chosen from plants where asbestos had not been in use and restricted to those without X-ray signs of chest disease. The primary type of asbestos used was chrysotile and the general dust level in the two decades 1950-1970 seems to have been around 10 mg/m3 while the asbestos fiber concentration averaged 2 fibers/ml. The mean differences between exposed and referents were statistically significant for forced vital capacity and forced expiratory volume, -0.25 and -0.30 liters, respectively, after adjustment for age, height, tracheal area, and smoking category. No significant differences were detected between those with and without pleural plaques. Smokers and never-smokers were similarly affected. In conclusion, the group exposed to dust with comparatively low asbestos fiber concentration had a minor impairment of lung function, mainly due to obstructive changes.

Several studies have shown an increased lung cancer mortality among Swedish metal and iron ore miners, as probably caused by exposure to radon and its daughters. An earlier study of zinc-lead miners has been updated. The results show a 16-fold increase in lung cancer mortality. Surprisingly, nonsmokers were more apt to develop lung cancer than smokers, but the induction-latency time was about nine years shorter on the average for the smokers. An explanation for these findings might be that smoking increases the thickness of the mucus layer and therefore protects the bronchial epithelium from alpha radiation, but it also promotes the development of cancer once induced by the radiation.

An earlier cohort study of Swedish railroad workers indicated a possible relationship between exposure to herbicides and an increased overall tumor morbidity and mortality. The cohort of 348 individuals has now been followed through October 1978. In this updated analysis of the causes of death among railroad workers, the observed number of tumor deaths was higher than expected, especially among individuals exposed in the earlier years of the study to both amitrol and phenoxy acids. However, the excess tumor mortality among persons exposed to amitrol became more moderate, and the earlier, slightly increased tumor mortality among people exposed to phenoxy acids more pronounced. No specific type of tumor predominated although there were three stomach cancers and three lung cancers. The result of the previous analysis of deaths among these railroad workers has been confirmed as to an excess of tumors, but the aspects of causal relationships to specific agents remain rather unclear, especially since workers exposed to a combination of amitrol and phenoxy acids seem to be the most seriously affected. However, the result, being in agreement with animal data and other epidemiologic studies, suggests a need for the careful handling of amitrol and phenoxy acids as increasingly suspicious carcinogens.