Environmental changes and their impact on human behaviour - Case study of the incidence of skin cancer.

Climatological research over the past two decades makes it clear that the Earth's climate will change. Climate change has many, mostly adverse, effects on the human health. Environmental anthropogenic changes represent significant health risks including factors that may increase probability and seriousness of skin cancer diseases. There are many scientific studies on skin cancer but only a few of them are focused on environment changes and their influence on the behaviour of humans, which may lead to skin cancer. The goal of the research was to analyse environment changes in the city of Brno (Czech Republic) and their influence on the behaviour of people and some skin diseases. A research hypothesis was set up that total increase in the incidence of skin diseases would be monitored. 1757 patients aged 25-65 years participated in the research. The analysis was performed based on measured (mean annual temperatures, average monthly temperatures, ultraviolet index values, and numbers of sunny days and sunny hours) data in 2011-2019. In order to monitor the trend, temperature data from 1961 to 2019 were evaluated too. The analysed data indicate that the trend of average monthly and annual temperatures observed was increasing in recent years. Moreover, based on data obtained from the analysed doctor's office it was found out that the incidence of skin diseases increased in the studied period. The main reasons to increase include excessive exposure to sun, extended average age of the population, ozone layer depletion, climatic and weather changes, increased migration and behaviour of people.

Inter strand crosslinks in DNA induced in vivo by percutaneous application of sulphur mustard to rats and mice.

Inter-strand crosslinks (ICL) in the DNA are regarded to be the main toxic lesions induced by sulphur mustard (SM). We have followed the induction of ICL in the DNA of different organs of Wistar rats and Balb/c or NMRI mice by the percutaneous application of SM using the modified (reverse) comet assay. Significant amounts of ICL were found in Balb/C lymphocytes, in bone marrow and liver cells after the dose of 80 mg/kg. A dose-dependent amount of ICL was induced in rats, with efficient induction in lymphocytes and spleen cells already after 5 mg SM/kg, indicating a higher susceptibility of rats to the DNA-damaging effect of SM compared with mice. A significant induction of ICL in other tested tissues (liver, bone marrow, colon epithelium) was seen at the dose of 20 mg/kg. The induced ICL were removed from the DNA during 48 h except for rats at the dose of 80 mg/kg. In fact, we observed that ICL are almost completely repaired in tissues of rats receiving high lethal doses. Results suggest that the unhooking of ICL, which we followed with the comet assay, may lead to the formation of another toxic DNA lesion during the repair process.