Reactive oxygen species (ROS) are normal products of a number of biochemical reactions and are important signaling molecules. However, at the same time, they are toxic to cells and have to be strictly regulated by their antioxidant systems. The etiology and pathogenesis of many diseases are associated with increased ROS levels, and many external stress factors directly or indirectly cause oxidative stress in cells. Within this context, the overexpression of genes encoding the proteins in antioxidant systems seems to have become a viable approach to decrease the oxidative stress caused by pathological conditions and to increase cellular stress resistance. However, such manipulations unavoidably lead to side effects, the most dangerous of which is an increased probability of healthy tissue malignization or increased tumor aggression. The aims of the present review were to collect and systematize the results of studies devoted to the effects resulting from the overexpression of antioxidant system genes on stress resistance and carcinogenesis in vitro and in vivo. In most cases, the overexpression of these genes was shown to increase cell and organism resistances to factors that induce oxidative and genotoxic stress but to also have different effects on cancer initiation and promotion. The last fact greatly limits perspectives of such manipulations in practice. The overexpression of GPX3 and SOD3 encoding secreted proteins seems to be the “safest” among the genes that can increase cell resistance to oxidative stress. High efficiency and safety potential can also be found for SOD2 overexpression in combinations with GPX1 or CAT and for similar combinations that lead to no significant changes in H₂O₂ levels. Accumulation, systematization, and the integral analysis of data on antioxidant gene overexpression effects can help to develop approaches for practical uses in biomedical and agricultural areas. Additionally, a number of factors such as genetic and functional context, cell and tissue type, differences in the function of transcripts of one and the same gene, regulatory interactions, and additional functions should be taken into account.

Studies investigating the taxonomic diversity and structure of soil bacteria in areas with enhanced radioactive backgrounds have been ongoing for three decades. An analysis of data published from 1996 to 2024 reveals changes in the taxonomic structure of radioactively contaminated soils compared to the reference, showing that these changes are not exclusively dependent on contamination rates or pollutant compositions. High levels of radioactive exposure from external irradiation and a high radionuclide content lead to a decrease in the alpha diversity of soil bacterial communities, both in laboratory settings and environmental conditions. The effects of low or moderate exposure are not consistently pronounced or unidirectional. Functional differences among taxonomic groups that dominate in contaminated soil indicate a variety of adaptation strategies. Bacteria identified as multiple-stress tolerant; exhibiting tolerance to metals and antibiotics; producing antioxidant enzymes, low-molecular antioxidants, and radioprotectors; participating in redox reactions; and possessing thermophilic characteristics play a significant role. Changes in the taxonomic and functional structure, resulting from increased soil radionuclide content, are influenced by the combined effects of ionizing radiation, the chemical toxicity of radionuclides and co-contaminants, as well as the physical and chemical properties of the soil and the initial bacterial community composition. Currently, the quantification of the differential contributions of these factors based on the existing published studies presents a challenge.

The present comprehensive study aimed to estimate the aftermath of oil contamination and the efficacy of removing the upper level of polluted soil under the conditions of the extreme northern taiga of northeastern European Russia. Soil samples from three sites were studied. Two sites were contaminated with the contents of a nearby sludge collector five years prior to sampling. The highly contaminated upper soil level was removed from one of them. The other was left for self-restoration. A chemical analysis of the soils was conducted, and changes in the composition of the soil zoocoenosis and bacterial and fungal microbiota were investigated. At both contaminated sites, a decrease in the abundance and taxonomic diversity of indicator groups of soil fauna, oribatid mites and collembolans compared to the background site were found. The pioneer eurytopic species Oppiella nova, Proisotoma minima and Xenyllodes armatus formed the basis of the microarthropod populations in the contaminated soil. A complete change in the composition of dominant taxonomic units was observed in the microbiota, both the bacterial and fungal communities. There was an increase in the proportion of representatives of Proteobacteria and Actinobacteria in polluted soils compared to the background community. Hydrocarbon-degrading bacteria—Alcanivorax, Rhodanobacter ginsengisoli, Acidobacterium capsulatum, and Acidocella—and fungi—Amorphotheca resinae abundances greatly increased in oil-contaminated soil. Moreover, among both bacteria and fungi, a sharp increase in the abundance of uncultivated organisms that deserve additional attention as potential oil degraders or organisms with a high resistance to oil contamination were observed. The removal of the upper soil level was partly effective in terms of decreasing the oil product concentration (from approximately 21 to 2.6 g/kg of soil) and preventing a decrease in taxonomic richness but did not prevent alterations in the composition of the microbiota or zoocoenosis.

Understanding the mechanisms producing low dose ionizing radiation specific biological effects represents one of the major challenges of radiation biology. Although experimental evidence does suggest that various molecular stress response pathways may be involved in the production of low dose effects, much of the detail of those mechanisms remains elusive. We hypothesized that the regulation of various stress response pathways upon irradiation may differ from one another in complex dose-response manners, causing the specific and subtle low dose radiation effects. In the present study, the transcription level of 22 genes involved in stress responses were analyzed using RT-qPCR in normal human fibroblasts exposed to a range of gamma-doses from 1 to 200 cGy. Using the alkali comet assay, we also measured the level of DNA damages in dose-response and time-course experiments. We found non-linear dose responses for the repair of DNA damage after exposure to gamma-radiation. Alterations in gene expression were also not linear with dose for several of the genes examined and did not follow a single pattern. Rather, several patterns could be seen. Our results suggest a complex interplay of various stress response pathways triggered by low radiation doses, with various low dose thresholds for different genes.