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Cadmium (Cd) is a nonessential transition metal and one of the most toxic environmental pollutants. Industrial, agricultural and urban activities are the main sources of Cd environmental contamination. Multiple deleterious effects of Cd exposure were reported for different cell types and living organisms in a great number of research papers. Cd bioaccumulation hazard is mediated by the relatively long half-life of this metal in an organism. For example, in mammals its half-life lasts for about 10–30 years. Cd exposure affects many tissues. However, some of them, including the central nervous system and sensory organs, are most susceptible to its toxicity. The harmful effects of Cd could be linked to oxidative stress generation and consequently intracellular signalling disruption. Since Cd induces redox imbalance the antioxidants could be a prospective tool to ameliorate Cd cytotoxicity. In present work, we have studied the protective efficacy of soluble curcumin on Cd-caused retinal pigment epithelium (RPE) cells viability, reactive oxygen species production, adhesive and extracellular matrix proteins expression, cell migration and parthanatos level. Low dose (5 µM) of soluble curcumin ameliorated all aforementioned indices of Cd-induced cytotoxicity. Curcumin has restored the RPE cells motility as well as fibronectin and E-cadherin expression. Therefore, the modulation of RPE adhesiveness could be regarded as a cytoprotective effect of curcumin. Furthermore, Cd-caused poly(ADP-ribose) polymerase-1 (PARP-1) suppression and cleaved PARP-1 upregulation were ameliorated by curcumin exposure. Therefore, the protective effect of soluble curcumin could be related, at least partially, to the modulation of PARP activity and inhibition of parthanatos flux. The observed results have demonstrated that low doses of soluble curcumin are a promising tool to protect RPE cells against Cd-caused retinal injury.

The present study was designed to evaluate the responsiveness of modulation of glial fibrillary acidic protein (GFAP) content and its fragmentation in the snake brain as a biomarker of local industrial pollution of aquatic ecosystems. Despite GFAP being a well known cytoskeleton marker of astrocytes’ reactivity in the brain of vertebrates, its expression in the snake brain remains insufficiently described. The GFAP expression and its fragmentation were detected using the immunoblot method in the snake brain. ROS level was determined with dichlorofluorescein diacetate fluorescence. The content of the glial fibrillary acidic protein (GFAP) of filament (cytoskeleton) and soluble (cytosol) fractions in the brain of dice snake Natrix tessellata from three ecosystems with different rates of industrial pollution were studied (two polluted and one clean control site). Characteristic increase in GFAP fragmentation was noted for the snakes from both the researched polluted sites. Significant increase in the content of the GFAP cleaved polypeptide fragments induced by industrial pollution exposure was confirmed in the snakes’ brains. Meaningful GFAP fragmentation was determined in snake brain astrocytes as an increase in cleaved fragments of 47–35 kDa molecular weight for both soluble and cytoskeletal GFAP fractions. We found significant abnormality in the ratio of the GFAP soluble fraction to the cytoskeletal one in contaminant-exposed dice snakes. It should testify to significant metabolic disturbance in nerve cells of the dice snakes. Furthermore, growth of reactive oxygen species level as the main cause of oxidative stress was determined in brains of the snakes exposed to environmental toxicity. Thus, astrocyte cytoskeleton disorders are associated with pollutant-induced redox imbalance in the snake brain. Despite the limited data on glial cell biology in the reptilian brain, the observed results prove that snake astrocytes can respond to the environmental toxicity using typical astroglial response. The presented results evidence that monitoring of molecular characteristics of glial cytoskeleton in dice snakes could be used as reliable biomarker of neurotoxicity and adverse effects of industrial pollution. Further studies are required to elucidate the role of astrocyte cytoskeleton in the response against neurotoxic contaminants.

Peptidoglycan is a universal component of bacterial walls that exerts various biological activities, including tumoricidal effect. Anti-cancer effect of various peptidoglycan fractions and their derivates is different. Muramyl pentapeptide (MPP) is the most complete building block of peptidoglycan. MPP can stimulate cell reactivity as well as other muropeptides. In the present study, we evaluated inhibitory MPP effect on viability and migration of glioblastoma cells U373MG. As markers of cell reactivity we determined the amounts of proteins PARP1 and NF-kB. MPP exposure induced decrease in viability and migration activity of glioblastoma cells. Besides, MPP treatment increased the amounts of PARP1 and NF-kB in a dose-dependent manner. Furthermore, NADH level in exposed glioblastoma cells was depleted as compared to control. Thus, MPP exhibits tumoricidal effect in glioblastoma cells U373MG via depletion NADH content and consequently metabolic energy level. Moreover, upregulation of the amounts of PARP1 and NF-kB in glioblastoma cells could be an important mechanism of the inhibition of cell migrative capability and the progress of the tumor. The obtained results evidenced that muramyl pentapeptide could initiate lack of migration via metabolic energy expenditure as a result of gliotypic reactivity. Further studies are actual and extremely required to clarify tumoricidal effect of this muropeptide in glia-derived tumors.

Copper sulphate pentahydrate (CuSO4∙5H2O) is widely used as a pesticide not only in agricultural but in aquaculture farming as well. Copper sulphate is a cheap chemical and able to contaminate the environment, especially water sources, which is crucial for fish harvesting and farming. The copper contamination in some areas is caused over decades because this pesticide has long been used everywhere. Copper ions inhibit invasive aquatic plants and many microorganisms but contaminate soil and natural water resources. The family of copper-containing chemicals is frequently used as algaecides in swimming pools. Despite the high toxicity of copper ions for fish in freshwater ponds, copper sulphate remains one of the prevalent pesticides in fish farming everywhere. High cytotoxicity and accumulation of the copper ions in sediments require study and calculation of the optimal dosage for its use as an antiseptic agent which will not have a detrimental effect on various tissue types of aquatic organisms. The main recognized mechanism which accompanies the toxic effect of copper ions is the generation of oxidative stress. Neural tissue cells are extremely susceptible to oxidative damage and the functions of the CNS are critical to the vitality of organisms. Glial cells maintain the structure and many vital functions of neurons. The cytoskeleton glial fibrillary acidic protein (GFAP), transcriptional nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and Poly(ADP-ribose) polymerase (PARP) are critical participants in a cellular response to a toxic agent impact. As this takes place, it could be applied in biomarking of heavy metal toxicity. In the presented study, we investigated the effects of copper ions on PARP, NF-kB, and GFAP expression in the Tigris scraper Capoeta umbla brain tissue. For 96 hours the fish were exposed to copper sulphate at sublethal concentrations, namely 1/2, 1/4 and 1/8 of the LD50 value. Western blot analysis of GFAP and PARP was used to assess further effects in the brain tissue. Every studied dose of copper significantly downregulated the expression of GFAP after 72 hours of treatment. In spite of the common increment in the GFAP content, 48 hours exposure to copper initiated the upregulation of that cytoskeleton marker. Moreover, treatment with copper sulphate induced several changes in the β-actin level, especially in the fish group treated for 72 hours. The observed effect of copper in the fish brain evidences the unspecific toxic effect of the copper ions in the brain tissue cells. The obtained results demonstrated meaningful disturbance in the expression of transcriptional factor NF-kB in the brain of the fish group exposed to copper. The changes found in the fish brain indicate the dose-dependent effect in a concentration range 185–740 µg/L of copper sulphate during 72 hours. However, the exposure to low dose of copper ions showed no effect in the fish group treated for 24 hours. Comparative analyses of the PARP content in the brain of fish exposed to copper for 72 hours was significantly less than in the groups treated with copper for both 24 and 48 hours. Thus, the copper ions in the dose range 185–740 µg/L can suppress PARP expression in a time-dependent manner. The results showed that copper ions could induce astroglial response accompanied by modulations of NF-kB and PARP-1 expression. The data obtained in this study suggest that copper sulphate has a significant effect on astrogliosis and DNA damage in the fish brain.