In recent decades, a global increase in the incidence of skin cancer, particularly squamous cell carcinoma (SCC), has been observed. To explore the pathogenesis and potential therapeutic approaches for this cancer type, in vivo studies employing various mouse models and ultraviolet (UV) light have been conducted. A comparative study on skin carcinogenesis across four hairless mouse models subjected to UV light exposure was initiated. The mouse strains utilized in this research were: SKH-hr1, SKH-hr2, SKH-hr2+ApoE, and immunodeficient Nude. Based on the various measured parameters, in contrast to the SKH-hr1, SKH-hr2+apoE and SKH-hr2 models were identified as the most appropriate.  The bark extract of Pinus maritima (PBE) was examined for SCC preventive action. It was evaluated in two different experimental animal tumor models induced by ultraviolet radiation (UVR) and combination of UVR with 7,12-dimethylbenz[a]anthracene. A significant decrease in the number of animals bearing tumors, increase in viability and delayed appearance of tumors were observed. Through immunochemical analysis, the expression of P-glycoprotein, multi-drug resistance-associated protein (MRP), and glucose (GLUT-1) transporters in SCC, SCC adjacent area, and normal skin tissues were examined. It was revealed that all assessed transporters were expressed across all skin tissues; however, expression levels were notably higher in tumor and tumor-adjacent areas compared to normal tissues. Male and female hairless SKH-2 mice were exposed for 10 months to cigarette smoke (CS) and/or UV light after administration or not of French maritime pine bark extract (PBE) to study the SCC induction and possible protection by PBE. The results showed that UV and CS were harmful and act synergistically inducing SCC, whereas PBE seems to protect skin against SCC. Type 1 and 2 diabetic, and nondiabetic male mice were exposed to UV radiation for eight months. Remarkably, Type 1 diabetic mice did not develop squamous cell carcinoma or pigmented nevi, contrary to normal and Type 2 diabetic skin. Type 1 diabetic mice showed protection against oxidative stress.

Ionising radiation damages DNA directly, or indirectly, causing water radiolysis and formation of free radicals. Indirect irradiation effects could be diminished in the presence of free radical scavengers, such as dimethyl sulfoxide (DMSO). Such conditions would allow the evaluation of direct radiation effects and provide a better understanding of cellular response to irradiation-induced damages. The goal of this study was to investigate the effects of low (γ-rays) and high linear energy transfer (LET) radiation (carbon ions) in non-small lung cancer cells HTB177. Cells were pre-treated with DMSO and irradiated with 60Co γ-rays and 62 MeV/u carbon ions, with doses ranging from 1-5 Gy. Results obtained by clonogenic survival and γ-H2AX foci assay showed that DMSO increased cell survival and decreased number of DNA damages, which points to radioprotective effect of DMSO. The contribution of direct and indirect radiation effects was estimated by the degree of protection (DP) in presence of DMSO. The values of DP rose in a concentration-dependent manner in all irradiated samples. In cells irradiated with γ-rays, 35% of damages were caused directly, while 65% of lesions could be attributed to indirect radiation actions. In presence of carbon ions, contribution of direct effects was 49%, while 51% of damage resulted from indirect radiation effects, showing that free radicals attain an important role in both low and high LET irradiations. The obtained results showed that DMSO can be used as a free radical scavenger to examine the direct and indirect effects on human cancer cells. The numerical Monte Carlo simulations allow modelling of direct and indirect irradiation actions in cancer cells with photons and hadrons. Therefore, this data will be used for validation and further improvement of numerical simulations in comparison to the data collected on different cell lines and irradiation energies, with the goal to improve therapeutic protocols.

Amphibians are the most threatened vertebrate class. Exposure to pesticides and climate change are considered pivotal factors in the global decline of their populations. Glyphosate-based formulations are the most widely used herbicides, but increasing evidence of their harmful effects, including oxidative stress in exposed organisms, has sparked a heated debate. Current climate prediction models assume a global temperature rise of 3 °C to 5 °C in the coming decades. In poikilotherms, any changes in ambient temperature are directly translated into changes in physiological and biochemical processes. Furthermore, elevated temperatures could intensify the toxic effects of pesticides present in the environment. The aim of this study was to examine the effects of low, environmentally realistic concentrations of glyphosate-based herbicides (30 µg/L active ingredient) and elevated temperature (optimal t1=19°C and increased t2=23°C) on glutathione content (GSH), antioxidant enzyme activities (SOD, CAT, GSH-Px, GR and GST), activity of acetylcholinesterase (AChE) and levels of oxidative damage (TBARS - lipid peroxidation and PC - protein carbonylation) in larvae of the Balkan crested newt (T. ivanbureschi). Our findings revealed that glyphosate had a significant effect on the activity of all antioxidative enzymes, with the exception of SOD. Herbicide and elevated temperature led to a significant increase in the activities of CAT, GSH-Px, GST, and GR, as well as GSH concentration. This response of the antioxidative defense system prevented oxidative damage to lipids and proteins. Glyphosate exhibited a neurotoxic effect by inhibiting AChE only at elevated temperatures, while no significant change occurred at the optimal temperature. The findings suggest the importance of examining the potentially harmful effects of glyphosate in different ecological contexts, such as an increase in average temperatures by several degrees predicted by future climate scenarios.