Cisplatin (Cis-diamminedichloroplatinum II, CP) is an important chemotherapeutic agent, useful in the treatment of several cancers, but with several side effects such as nephrotoxicity. The present study investigated the possible protective effect of selenium (Se) against CP-induced oxidative stress in the rat kidneys. Male Wistar albino rats were injected with a single dose of cisplatin (7 mg CP/kg b.m., i.p.) and selenium (6 mg Se/kg b.m, as Na₂SeO₃, i.p.), alone or in combination. The obtained results showed that CP increased lipid peroxidation (LPO) and decreased reduced glutathione (GSH) concentrations, suggesting the CP-induced oxidative stress, while Se treatment reversed this change to control values. Acute intoxication of rats with CP was followed by statistically significant decreased activity of antioxidant defense enzymes: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR) and glutathione-S-transferase (GST). Treatment with Se reversed CP-induced alterations of antioxidant defense enzyme activities and significantly prevented the CP-induced kidney damage.

The study’s objective was to obtain silver nanoparticles (SVAgNP and FUAgNP) using aqueous extracts of Salvia verticillata and Filipendula ulmaria. The optimal conditions for nanoparticle synthesis were determined and obtained; nanoparticles were then characterized using UV-Vis, Fourier-transform infrared spectroscopy (FTIR), X-ray powder diffraction (XRD), Dynamic Light Scattering (DLS), Scanning Electron Microscopy with Energy Dispersive Spectroscopy (SEM/EDS). SVAgNP and FUAgNP possessed a crystalline structure with 48.42% and 60.41% silver weight, respectively. The highest percentage of nanoparticles in the solution had a diameter between 40 and 70 nm. In DPPH˙ and ABTS˙⁺ methods, FUAgNP (IC₅₀ 15.82 and 59.85 µg/mL, respectively) demonstrated a higher antioxidant capacity than SVAgNP (IC₅₀ 73.47 and 79.49 µg/mL, respectively). Obtained nanoparticles also showed pronounced antibacterial activity (MIC ˂ 39.1 µg/mL for most of the tested bacteria), as well as high biocompatibility with the human fibroblast cell line MRC-5 and significant cytotoxicity on some cancer cell lines, especially on the human colon cancer HCT-116 cells (IC₅₀ 31.50 and 66.51 µg/mL for SVAgNP and FUAgNP, respectively). The nanoparticles demonstrated high catalytic effectiveness in degrading Congo red dye with NaBH₄. The results showed a rapid and low-cost methodology for the synthesis of AgNPs using S. verticillata and F. ulmaria with promising biological potential.

Summary: The aim of this study was to investigate the protective effects of oestradiol (E2, 4 mg kg^-1 b.w. i.p.) against cadmium-induced (Cd, 2 mg kg^-1 b.w. i.p.) blood changes in rats. Cadmium induced a significant decline in haemoglobin, haematocrit, and total erythrocyte, lymphocyte, and thrombocyte count, whereas total leukocytes and granulocytes increased. A significant increase was also observed in serum cholesterol, triglycerides, glucose, AST, and ALT activities, whereas total protein and albumin levels dropped significantly. Administration of E2 in combination with Cd alleviated most of these adverse effects. In terms of oxidative stress, Cd significantly increased oxygen-free radicals (O₂ •- and H₂O₂) in neutrophils and lipid peroxidation in erythrocytes, whereas E2 treatment reversed these changes to control values. Acute Cd poisoning significantly lowered antioxidant enzyme (SOD and CAT) activity and the level of non-enzymatic antioxidants (GSH and vitamin E), while increasing in GSSG. Treatments with E2 reversed Cd-induced effects on the antioxidant defences and significantly lowered Cd-induced oxidative damage in erythrocytes. This study suggests that exogenous E2 effectively restores redox balance in rat erythrocytes and counters adverse haematological and biochemical effects of Cd poisoning. It also improves the antioxidant capacity of erythrocytes, acting in synergy with endogenous antioxidants.

Cadmium (Cd) is a major environmental pollutant, which exerts adverse effects mainly by inducing oxidative stress. Coenzyme Q₁₀ (CoQ₁₀) and vitamin E (VE), naturally occurring antioxidants, improve health condition by inactivating free radicals and enhancing antioxidative defence. The aim of our study was to investigate the protective role of CoQ₁₀ and/or VE pretreatment against Cd-induced haematotoxicity. Wistar albino rats were intramuscularly injected with CoQ₁₀ (20 mg/kg b.w.) and/or VE (20 IU/kg b.w.) or with saline (control group). After 24 h, Cd was injected intraperitoneally (0.4 mg/kg b.w.) and 1 day after, animals were sacrificed. Acute Cd intoxication caused significant changes in haematological and biochemical parameters and altered the glutathione cycle, leading to the formation of lipid peroxidation, while the concentrations and activities of antioxidants (vitamins C and E, superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase) were decreased. CoQ₁₀ and/or VE significantly maintained these values to near-normal levels, afforded additional protection by reducing lipid peroxidation and improved the levels of antioxidants in the blood. Plasma CoQ₁₀ and VE levels negatively correlated with oxidative damage parameters while positively correlated with antioxidative defence parameters. Regarding their effects, CoQ₁₀ and VE were in synergistic interaction. The present study suggested that CoQ₁₀ and VE combination may be beneficial in protecting from Cd-induced haematotoxicity and may be used as a preventive against acute Cd intoxication of exposed people.