One of the most influential factors in the process of environmental pollution is road transport, i.e. emission of gaseous pollutants from road vehicles. An especially pronounced problem is the air pollution in urban areas, with a high concentration of road vehicles having very different driving regimes. The largest influence on pollutants emission of road vehicles is that of: − Technical and technological solutions used in internal combustion engines, which is directly connected with the given vehicle's particular year of production, − Engine type, − Fuel type and quality, − Vehicles concentration and use in certain areas, − Driving regimes, etc. For the purpose of getting a complete image of influences of road vehicles on pollutants emission, we have analyzed pollutants emission in an urban area with 100,000 registered vehicles, 60 % of which had diesel engines, with quite unfavorable age structure. The results have been compared with similar results in the Western European countries. Also, a review of modern technical accomplishments used in conventionally fueled vehicles for satisfying the European environmental legislation has been done in this paper. A special attention has been paid to alternative fuels, with the emphasis on the presently used fuels. Technical solution for the utilization of natural gas, as a very promising alternative fuel, and its influence on pollutants emission, has also been presented.

We have studied the consequences of two homoplasmic, pathogenic point mutations (T7512C and G7497A) in the tRNASer(UCN) gene of mitochondrial (mt) DNA using osteosarcoma cybrids. We identified a severe reduction of tRNASer(UCN) to levels below 10% of controls for both mutations, resulting in a 40% reduction in mitochondrial protein synthesis rate and in a respiratory chain deficiency resembling that in the patients muscle. Aminoacylation was apparently unaffected. On non-denaturating northern blots we detected an altered electrophoretic mobility for G7497A containing tRNA molecules suggesting a structural impact of this mutation, which was confirmed by structural probing. By comparing in vitro transcribed molecules with native RNA in such gels, we also identified tRNASer(UCN) being present in two isoforms in vivo, probably corresponding to the nascent, unmodified transcripts co-migrating with the in vitro transcripts and a second, faster moving isoform corresponding to the mature tRNA. In cybrids containing either mutations the unmodified isoforms were severely reduced. We hypothesize that both mutations lead to an impairment of post-transcriptional modification processes, ultimately leading to a preponderance of degradation by nucleases over maturation by modifying enzymes, resulting in severely reduced tRNASer(UCN) steady state levels. We infer that an increased degradation rate, caused by disturbance of tRNA maturation and, in the case of the G7497A mutant, alteration of tRNA structure, is a new pathogenic mechanism of mt tRNA point mutations.