<p style="text-align: justify;"><span class="a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none">Halogenated boroxine is an important enzyme inhibitor with potential applications in cancer therapy. This study aimed to evaluate its effects on hematological parameters in rats</span><span class="a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none"> <em>in vivo</em></span><span class="a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none"><em> </em>and creatine kinase activity </span><em><span class="a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none">in vitro</span></em><span class="a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none">. Halogenated boroxine, administered either intraperitoneally (IP) or orally, induced route-dependent changes in hematological parameters compared with controls. IP administration significantly increased neutrophils, mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC), while decreasing hematocrit (HCT). In contrast, oral administration significantly decreased lymphocytes and increased basophils, while other hematological parameters remained unchanged. These effects were more pronounced following IP administration. </span><em><span class="a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none">In vitro</span></em><span class="a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none">, halogenated boroxine exhibited competitive inhibition of creatine kinase without pre-incubation, whereas after a 30-minute pre-incubation, the inhibition pattern indicated a non-competitive mechanism. Further analysis showed a time-dependent shift in creatine kinase inhibition mechanism following pre-incubation, characterized by a decrease in maximum reaction velocity (V</span><span class="a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none font-size-modifier vertical-align">max</span><span class="a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none">), while the Michaelis constant (K</span><span class="a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none font-size-modifier vertical-align">m</span><span class="a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none">) remained unaltered. These findings show that halogenated boroxine modulates specific hematological parameters and inhibits creatine kinase activity, with effects depending on the route of administration and experimental conditions.</span></p>

Five neutral heteroleptic mononuclear vanadium(IV) hydrazone complexes ([VOL(bpy)]), derived from 2-hydroxy-5-methylacetophenone and various acid hydrazides (furoic, thiophene, benzoic, nicotinic, and isoniazid), were synthesized and shown to exhibit improved antidiabetic efficacy in streptozotocin-induced diabetic rats, with reduced toxicity and minimal bioaccumulation compared to maltolato- and picolinato-based vanadium species. Structural identity was established by spectroscopic methods. Crystal structures were obtained for four complexes, providing insight into their solid-state chemistry. Stability studies in simulated intestinal and gastric fluids showed that the complexes largely retained their integrity under intestinal conditions, whereas decomposition occurred in the highly acidic gastric environment within several minutes. In vivo experiments revealed a structure-antihyperglycemic activity relationship. The nicotinic-containing complex showed the highest activity, reducing blood glucose levels by 67% within 7 days of treatment, while the remaining complexes improved glycemic control by more than 50%. Bioaccumulation studies demonstrated <1.1% uptake in the liver and kidneys and negligible accumulation in the brain. The presented vanadium compounds enhance antidiabetic potential by addressing key limitations, particularly bioaccumulation and toxicity, associated with vanadium agents previously evaluated in clinical trials.

Abstract The toxicity of vanadium(IV) acetophenone–isoniazid hydrazone complexes (V1–V4) was evaluated in Artemia salina. Nauplii were exposed for 24–72 h at 1, 5, 10, and 50 mg/L. Responses were concentration dependent: reduced hatching, increased mortality, and morphological changes (appendage and carapace defects, intestinal accumulation). Toxicity ranked by substituent: V2 (F) most toxic (≈60% mortality at 72 h, 50 mg/L), V3 (Cl) intermediate, V1 (H) and V4 (Br) lower (near 30% under the same conditions). Findings were compared with data from streptozotocin-induced diabetic Wistar rats. V4, moderately toxic in Artemia, showed the strongest antihyperglycemic effect (ca. 72% glucose reduction to near-normoglycemia) and the lowest renal bioaccumulation. V2 aligned with unfavorable renal/hepatic markers. V1 was well tolerated in Artemia and produced moderate glucose lowering with lipid improvements. V3 gave intermediate efficacy but higher bioaccumulation and hematological deviations. A. salina is a suitable early toxicity screen that, combined with mammalian data, reveals structure–activity–toxicity relationships. Halogen substitution modulates both efficacy and toxicity: Br provides the most balanced profile, F the highest liability, and H the safest but least potent. V4 (Br) emerges as the leading candidate for further preclinical study. Graphical abstract

A novel heterobimetallic ruthenium(II)–gold(I) complex featuring a bridging bis(diphenylphosphino)butane (dppb) ligand was prepared and fully characterized. Single-crystal X-ray diffraction revealed a piano-stool geometry around Ru(II) with η6-cymene, two chlorido ligands, and one phosphorus atom from dppb, while the Au(I) center adopts a linear P–Au–Cl coordination. Structural integrity in the solution was confirmed by 1D and 2D NMR spectroscopy, while solution behavior was further monitored by variable solvent 31P NMR and UV/Vis spectroscopy, indicating that the organometallic Ru–arene core remains intact, whereas the chlorido ligands coordinated to Ru exhibit partial lability. Complementary characterization included elemental analysis, FTIR, and UV/Vis spectroscopy. Spectrofluorimetric and FRET analyses showed that Au(dppb), Ru(dppb), and the heterobimetallic AuRu complex bind to BSA with apparent constants of 1.41 × 105, 5.12 × 102, and 2.66 × 104 M−1, respectively, following a static quenching mechanism. In vivo biological evaluation in Wistar rats revealed no significant hepatotoxicity or nephrotoxicity, with only mild and reversible histological alterations and preserved hepatocyte nuclear morphology. Hematological analysis indicated a statistically significant reduction in leukocyte populations, suggesting immunomodulatory potential, while elevated serum glucose levels point to possible endocrine or metabolic activity. These findings highlight compound structural stability and intriguing bioactivity profile, making it a promising platform for further organometallic drug development and testing.

Four new heteroleptic neutral paramagnetic mononuclear oxidovanadium(IV) complexes, designated as [VOL(phen)], where L corresponds to acetophenone isoniazid hydrazone or its 5-halogenated derivatives and phen stands for 1,10-phenanthroline, were synthesized and thoroughly characterized using chemical analysis, various spectroscopic techniques, and diffraction methods. Single-crystal X-ray diffraction revealed the molecular and crystal structures of two complexes, showing an octahedral coordination environment around the vanadium(IV) center. The coordination includes a tridentate ONO donor hydrazone ligand in its deprotonated enol-imine form, 1,10-phenanthroline as a bidentate NN donor ternary ligand, and one terminal oxygen atom. The biochemical and hematological effects of these complexes were evaluated in a streptozotocin-induced diabetic rat model. All synthesized complexes showed cholesterol-lowering effects compared to the diabetic rat group, with the vanadium complex lacking a substituent on the acetophenone ring of hydrazone showing the strongest effect. Complexes exhibited comparable and significant antidiabetic activity in vivo, effectively reducing hyperglycemia within 1 week of treatment. Additionally, the histopathological effects of complex (4) on liver, kidney, and brain tissues were investigated. All four complexes were found to have low bioaccumulation levels, with total absolute bioaccumulation in all tested organs less than 0.35% of the administered dose.

The environmental fragmentation of plastics generates a mixture of plastic particles of various sizes, which frequently co-occur with other mobile and persistent environmental pollutants. Despite the prevalence of such scenarios, the interaction between micro- and nanoplastics (MNPs) and their combined effects with environmental pollutants, such as highly toxic hexavalent chromium (Cr(VI)), remain almost entirely unexplored in mammalian species. This study demonstrated that nanoplastic and microplastic particles co-aggregate and together influence Cr bioaccumulation patterns and related physiological alterations in rats. Following a four-week repeated intragastric exposure of Wistar rats to MNPs and Cr(VI), either alone or in combination, MNPs significantly enhanced Cr bioaccumulation in the liver, heart, brain, and skin. Under co-exposure conditions, Cr(VI) was the primary driver of cellular effects observed in the blood, including shifts in immune cell subpopulations (e.g., neutrophils, lymphocytes) and alterations in red blood cell indices, while serum biochemistry reflected limited physiological stress. MNPs per se decreased creatine kinase activity and increased cholesterol levels. In summary, polystyrene MNPs increase Cr(VI) distribution and bioavailability, but co-exposure does not uniformly exacerbate toxicity. Instead, their interaction may selectively alter physiological responses, emphasizing the need for a deeper understanding of their combined effects and potential health risks.

Background/Aim. Rheumatoid arthritis (RA) is a systemic autoimmune disease that can cause destructive joint disease and progressive disability. The diagnosis of RA is based on laboratory and clinical evidence, which includes the analysis of inflammatory markers, hematological, and biochemical parameters. Methods. Fifty patients diagnosed with RA without methotrexate (MTX) therapy and 50 patients with therapy (MTX, 7.5 mg/week; after three months prednisolone 10 mg/day) were included in this study. After six months of therapy, inflammatory biomarkers, hematological, and biochemical parameters were analyzed. Results. Inflammatory biomarkers: sedimentation rate (SE), C-reactive protein (CRP), and anti-cyclic citrullinated peptide (anti-CCP) are significantly lower in the group of patients on therapy compared to patients without MTX therapy. Significant differences were not found for the rheumatoid factor (RF). Significant differences were not found for hematological parameters between the compared groups. Analysis of serum biochemical parameters showed significant differences for aspartate aminotransferase (AST) and iron values. In patients without MTX therapy, the incidence of anemia was recorded in 68%, which is significantly higher than the incidence of 32% in patients with therapy. Conclusion. Prescribed therapy has shown effectiveness in the treatment of RA and reduction of the inflammatory process. The success of the treatment depends on the timely diagnosis of RA. Postponement of therapy and late-detected disease prolongs therapy treatment and often requires a combination of several drugs.

Abstract CCl4 causes oxidative injury, fatty degeneration, fibrosis of the liver, renal failure, and even hepatocellular and renal carcinoma. Certain substances have the potential to neutralize the harmful effects of CCl4, so it will lead to numerous beneficial effects. Melatonin (MEL) is a powerful antioxidant that regulates circadian rhythm and has beneficial effects on organism; tryptophan (TRP) is its precursor necessary for the synthesis of MEL. The aim of the current study was to determine whether MEL and TRP, have protective effects during subchronic application of CCl4 to the liver and kidneys. Results suggest that CCl4 led to decrease of total proteins, albumins, globulins, erythrocytes, hemoglobin, and hematocrit; and increase of creatinine, AST, ALT values, and leukocytes. MEL and TRP both showing protective effects on regulation of serum proteins, albumins, globulins, A/G, AST, ALT, and creatinine levels. TRP had been shown to have potential in regulation of disbalanced hematological parameters caused by CCl4. TRP had beneficial effects on hepatocyte morphology in term of beaded chromatin and preserved cell morphology. Overall, oral supplementation of TRP had better protective effects on liver/kidneys compared to MEL.