Solution synthesis afforded five novel neutral heteroleptic octahedral paramagnetic mononuclear oxidovanadium(IV) complexes of general composition [VO(bpy)L], where L is a dianionic tridentate ONO-donor hydrazone ligand derived from 2-furoic acid hydrazide and salicylaldehyde and its 5-substituted derivatives. Characterization was carried out by elemental analysis, mass spectrometry, infrared, electron, NMR, and EPR spectroscopy, cyclic voltammetry and conductometry. The molecular and crystal structure of the complex with 5-chloro-salicylaldehyde 2-furoic acid hydrazone (2) was determined. The quantum chemical properties of the vanadium complexes were studied at B3LYP and M062X levels with the lanl2dz basis set using Gaussian. Additionally, Swiss-ADME analysis was performed and complex (4), featuring a 5-nitro substituent on the hydrazone ligand, was selected for further investigation. The effects of the in vivo application of the complex on selected biochemical parameters in healthy and diabetic Wistar rats were investigated. Strong antidiabetic effect associated with moderate hypoalbuminemia was observed. Furthermore, the interaction of complexes with BSA was studied by spectrofluorimetry. A significant conformational change of BSA in the presence of vanadium complexes was found. Synchronous fluorescence spectra revealed significant changes in the tyrosine microenvironment of BSA. The FRET analysis was also used and the non-radiative process of energy transfer is elucidated. Thermodynamic data suggest van der Waals forces and hydrogen bonding as predominant binding modes of complexes to BSA.

Nickel (Ni) is a widespread environmental pollutant commonly released into effluent due to industrial activities, the use of fuels, or wastewater disposal. Many studies confirm the toxic effects of this heavy metal. However, there is a lack of knowledge and data on bioaccumulation patterns in tissues as well as cellular and molecular responses following the exposure of living organisms to Ni. In this study, Japanese quails were exposed to low (10 μg/L) and high (2000 μg/L) Ni concentrations in the form of nickel(II) chloride via drinking water. Sub-chronic exposure lasted 30 days while nominal concentrations represented average Ni content in drinking water (low dose) and average Ni levels in highly polluted aquatic environments (high dose). It was revealed that a high dose of Ni was correlated with increased water intake and decreased body weight. Overall, Ni exposure induced the development of microcytic anemia and alterations in measured blood indices. Moreover, Ni exposure impaired immunological activation as seen through the increased number of the white blood cells, increased heterophile/lymphocyte (H/L) ratio, and pronounced thrombocytosis. Ni elicited changes in the albumin, glucose, cholesterol, and triglyceride serum levels in a concentration-dependent manner. Alterations of plasma protein fractions suggested liver functional impairment while high levels of urea and creatinine indicated potential kidney injury. Granulation of heterophiles and an increase in erythroblasts in the bone marrow showed that the hematopoietic tissue was also impacted by Ni toxicity. On average each quail bioaccumulated 5.87 μg of Ni per gram of tissue. Moreover, the distribution and bioaccumulation of Ni in terms of relative concentration were as follows: feathers > kidneys > heart > liver > pectoral muscles. Assessed bioaccumulation levels and associated cellular and metabolic alterations have revealed new multilayer toxicological data that will help in the extrapolation of Ni toxicity in other vertebrates, including humans.

Carbon tetrachloride (CCl4) is known to have hepatotoxic and nephrotoxic effects. During the two‐month CCl4 exposure of Wistar rats, propolis extract (PE) and royal jelly (RJ) were added in order to test the potential protective effect against hepato‐renal injury. Ketonuria, proteinuria, high creatinine and urea levels are the result of CCl4‐induced nephrotoxicity. Severe disorders of hematological indicators indicate anemia; high values of leukocytes indicate inflammatory condition. Cytogenetic impairments in hepatocytes, aggregation of platelets, and hypoproteinemia indicate severe liver impairment. Results suggest a more significant protective role of RJ compared to PE. Both extracts regulated proteinuria, ketonuria, hypoproteinemia and reduced platelet aggregation in the hepatic circulation. The increase in the number of erythrocytes (RBC) suggest protective effects against anemia; the decrease in the number of leukocytes can be linked to anti‐inflammatory effects. PE and RJ have a beneficial effect against hepato‐renal injury, anemia and anti‐inflammatory conditions caused by CCl4.

Sodium benzoate (SB) as an additive in various food products prevents the growth of microbes. Although SB is considered safe, many studies have reported adverse effects. The aim of this study was to investigate the effect of dandelion extract on cell damage and hematological and biochemical disorders induced by SB in male albino rats. Different doses of SB (200 and 600 mg/kg) and ethanolic dandelion root extract (D) (40 mg/kg) were used in a 2‐week treatment of rats. Rat mortality and a higher frequency of behavioral alterations such as apathy, anxiety, and aggression have been reported at a higher dose of SB. Changes in urine pH, proteinuria, nitrituria, and bilirubinemia caused by SB were regulated by adding dandelion extract. Analysis of specific serum and urine parameters, as well as microscopic analysis of hepatocytes, showed liver and kidney failure. Anemia associated with hemolytic disorder due to erythrocyte impaired the presence of acanthocytes, and decreased values of erythrocyte blood count, hemoglobin concentration, average red blood cell size, hemoglobin amount per red blood cell, and mean corpuscular hemoglobin concentration were caused by SB treatment. As a dietary supplement, dandelion extract can be useful in the prevention of SB‐induced liver and kidney injury, and also a remedy against induced anemia, neutropenia, thrombocytopenia, hyperproteinemia, hyperglycemia, and reduction of inflammatory responses.

The purpose of this study was to explore possible protective effects of vitamin D3 on serum glucose concentration, body weight and histopathology of pancreas and liver. Animals were divided into 3 groups: Control group (n=6), streptozotocin (STZ) group (n=6) and streptozotocin + vitamin D3 (STZ+D3) group (n=6). Rats in the STZ+D3 group starting from the 7th day of experiment were given vitamin D3 for 14 days. Glucose levels and body weight were measured on the 1, 7, 14 and 21st day of experiment. Qualitative histological analysis of pancreas and liver was done using the light microscope with a digital camera. Differences between the groups were tested by one-way analysis of variance (ANOVA) followed by Dunnett's posttest. Differences in repeated measures were tested using paired t-test. On day 14 and 21, blood glucose level in STZ+D3 group was significantly higher compared to the control group of animals but significantly lower than the glucose level registered in STZ group of rats. On day 14 and day 21, body weight in STZ rats was significantly lower compared to weight in STZ+D3 and control groups of rats. Morphological changes, such as shrinkage of islets, vacuolation of both endocrine and exocrine cells, were observed in pancreas of STZ group of animals but were nearly absent in STZ+D3 rats. Similarly, STZ+D3 group of rats showed preserved liver histoarchitecture. Obtained results suggest that vitamin D3 treatment reduces hyperglycemia, exerts beneficial effects on body weight and alleviates histopathological changes in pancreas and liver in STZ-induced diabetic rats.

ABSTRACT Endangerment of fish habitats worldwide is a global problem. Breeding fish in restocking hatcheries is important for bioconservation of many fishes. Analysis of biochemical and hematological parameters provides important information on spawning performance and fish health. Variations of different serum biochemical constituents and increase in body length and mass of West Balkan trout were analyzed during spawning and postspawning. High body weight deviations of males were found in both periods. The body length and weight of males is higher compared to females. After spawning, higher growth was observed in males. Biochemical values are higher in females in relation to males. Low values of glucose, chloride, and potassium are present in the spawning phase. Decreases in protein, triglycerides, cholesterol, AST, sodium, and calcium levels were found in postspawning. Serum biochemical constituents of females vary significantly compared to males. Serum markers indicate a strong association with metabolic processes, which allows for better nutritional control and management of environmental factors, especially the presence of organic particles in the broodstock.

Hexavalent chromium (Cr(VI)) is an environmental pollutant with vast mutagenic and carcinogenic potential. Various past and recent studies confirm the deleterious effects of Cr(VI) in different models, from invertebrates to mammalians. However, there is a lack of studies that comprehensively assess and correlate Cr(VI) accumulation patterns and the resulting physiological responses. Here we used an attractive toxicological model, male Japanese quail (Coturnix japonica), as an alternative probing system to evaluate Cr(VI) accumulation in the vital organs, including the brain, heart, kidneys, liver, and testes after 20 days of exposure to 1.2 μg/mL and 2.4 μg/mL potassium dichromate-K2Cr2O7 ingested in the form of drinking water. The observed effects were correlated with the shift in immune system readiness, hematological indices, serum biochemistry and enzyme activity. Regardless of the exposure dose, the Cr(VI) distribution and accumulation pattern in terms of relative Cr(VI) concentration in tissues was: testes > kidneys > liver > heart > brain. Moreover, Cr(VI) triggered the development of microcytic and hypochromic anemia and reduced the immune system's readiness to cope with challenges. Besides, serum biochemistry presented significant shifts, including reduction of serum electrolytes and proteins and an increase in creatine kinase (CK) and lactate dehydrogenase (LDH) activity. Our study provides novel toxicological data that can be translated to higher animal models to help in the extrapolation of Cr(VI) toxicity in humans.