The triple exposure nexus of microplastic particles, plastic-associated chemicals, and environmental pollutants from a human health perspective.

The presence of microplastics (MPs) is increasing at a dramatic rate globally, posing risks for exposure and subsequent potential adverse effects on human health. Apart from being physical objects, MP particles contain thousands of plastic-associated chemicals (i.e., monomers, chemical additives, and non-intentionally added substances) captured within the polymer matrix. These chemicals are often migrating from MPs and can be found in various environmental matrices and human food chains; increasing the risks for exposure and health effects. In addition to the physical and chemical attributes of MPs, plastic surfaces effectively bind exogenous chemicals, including environmental pollutants (e.g., heavy metals, persistent organic pollutants). Therefore, MPs can act as vectors of environmental pollution across air, drinking water, and food, further amplifying health risks posed by MP exposure. Critically, fragmentation of plastics in the environment increases the risk for interactions with cells, increases the presence of available surfaces to leach plastic-associated chemicals, and adsorb and transfer environmental pollutants. Hence, this review proposes the so-called triple exposure nexus approach to comprehensively map existing knowledge on interconnected health effects of MP particles, plastic-associated chemicals, and environmental pollutants. Based on the available data, there is a large knowledge gap in regard to the interactions and cumulative health effects of the triple exposure nexus. Each component of the triple nexus is known to induce genotoxicity, inflammation, and endocrine disruption, but knowledge about long-term and inter-individual health effects is lacking. Furthermore, MPs are not readily excreted from organisms after ingestion and they have been found accumulated in human blood, cardiac tissue, placenta, etc. Even though the number of studies on MPs-associated health impacts is increasing rapidly, this review underscores that there is a pressing necessity to achieve an integrated assessment of MPs' effects on human health in order to address existing and future knowledge gaps.

Assessing chromium toxicity across aquatic and terrestrial environments: a cross-species review.

Chromium (Cr) toxicity, even at low concentrations, poses a significant health threat to various environmental species. Cr is found in the environment in two oxidation states that differ in their bioavailability and toxicity. While Cr(III) is essential for glucose metabolism, the oxyanion chromate Cr(VI) is mostly of anthropogenic origin, toxic, and carcinogenic. The sources of Cr in the environment are multiple, including geochemical processes, disposal of industrial waste, and industrial wastewater. Cr pollution may consequently impact the health of numerous plant and animal species. Despite that, the number of published studies on Cr toxicity across environmental species remained mainly unchanged over the past two decades. The presence of Cr in the environment affects several plant physiological processes, including germination or photosynthesis, and consequently impacts growth, and lowers agricultural production and quality. Recent research has also reported the toxic effects of Cr in different aquatic and terrestrial organisms. Whereas some species showed sensitivity, others exhibited tolerance. Hence, this review discusses the understanding of the ecotoxicological effect of Cr on different plant and animal groups and serves as a concise source of consolidated information and a valuable reference for researchers and policymakers in an understanding of Cr toxicity. Future directions should focus on expanding research efforts to understand the mechanisms underlying species-specific responses to Cr pollution.

Therapeutic benefit of oregano oil in the acute idiosyncratic hepatotoxicity induced by carbon tetrachloride in rats: Adverse effects of high dose of oreganum.

Toxicity caused by carbon tetrachloride (CCl4) can lead to serious liver injury. The aim of the study is to investigate the protective effects of oregano oil (Origanum minutiflorum extract oil) against CCl4-induced liver injury. Two doses of oregano oil were used in the experiment: a low dose (LD; 20 mg/kg) and a high dose (HD; 60 mg/kg) during 2 weeks. CCl4 caused severe liver damage, nucleolus destruction in hepatocytes and cytogenetic changes in the nucleus. Indirectly, CCl4 causes decreased protein synthesis and significantly high creatinine and urea values. Hematological disorders have been recorded, such as decreased RBC and hemoglobin concentration, increased WBC and deformability of the erythrocyte membrane. Both doses of oregano oil had protective effects. Improved protein synthesis and high globulins level, creatinine and urea were found in both groups. Cytogenetic changes in the nucleus of hepatocytes were reduced. A high dose of oregano oil had maximal protective effects for RBC, but a very weak effect on hemoglobin synthesis. Also, WBC and lymphocyte values were low. Origanum stimulates protein synthesis and recovery of hepatocytes after liver injury, reduces the deformability of the erythrocyte membrane. High doses of oregano oil decreased WBC and lymphocytes which may lead to a weakening of the immune response. However, high doses are more effective against severe platelet aggregation than low doses, suggesting an effective treatment against thrombocytosis.

Aronia melanocarpa (Michx.) Elliott 1821 Extract Has Moderate Ameliorative Influence on Biochemical and Hematological Parameters in Gentamicin-Induced Nephropathy in Wistar Rats.

Gentamicin (GM) is an aminoglycoside antibiotic used to treat bacterial infections. Nephrotoxicity refers to the impairments of the kidneys caused by the use of GM and can result in decreased kidney function and in severe cases, kidney failure. Aronia melanocarpa extract (AME), also known as the black chokeberry, has been used for its protective effects on the kidneys. AME concentration of 3.38 mg/kg (max antioxidant activity in vitro) was used to determine its effectiveness against induced nephropathy during 30 days. GM treatment caused significant hypoalbuminemia and high values of globulins, creatinine, and urea compared to the control group. GM application lead to hemolysis occurrence, echinocytosis, and platelets aggregation. Significantly high values of segmented neutrophils and low values of non-segmented neutrophils were recorded in the blood of rats treated with chokeberry extract (AME). In the pre-treatment (AME + GM), severe hypochromic anemia and a significant improvement in hematological parameters, as well as a reduction of anemia in the post-treatment (GM + AME), were noted. Post-treatment AME also significantly regulates urea and creatinine values. Statistically significantly low hemoglobin values were found in all groups treated with AME. Current study suggests that compounds in the AME have a moderate beneficial effect against renal injury and anti-inflammatory properties that may help protect the kidneys from injury caused by GM.

Impact of dietary supplementation with chokeberry (Aronia melanocarpa, Michx.) on tetrachloride-induced liver injury in Wistar rats: Hematological and biochemical implication.

In the current study, we assessed the hematological/biochemical alterations, histopathological changes in the liver, and blood cell disorders in Wistar rats exposed to a toxic concentration of carbon tetrachloride (CCl4 ) and the potential protective effect of a 30-day oral extract of chokeberry (Aronia melanocarpa, AM). The concentration of AM (3.38 mg/kg) obtained by quantitative purification from AM fruit showed the highest antioxidant activity (AOA) in vitro and was used for oral ingestion. In addition to high AOA, high values of total phenols (85.334 mg/g), total phenolic acid (606.95 mg/g), total flavonids (22.10 mg/g), and total anthocyanins (11.01 mg/g) were recorded in chokeberry extract. CCl4 treatment caused serious liver injury, hepatocyte and blood cell impairment. AM extract given to rats before CCl4 application had a moderate hepatoprotective effect in comparison to after CCl4 application. White blood count and leukocytes were significantly altered by CCl4, however, the protective role of AM in leukocyte disorders was not established. A high number of microcytes, stomatocytes, anisocytes, and hemolyzed erythrocytes during CCl4 exposure was reduced by AM extract. Flower erythrocytes in the AM + CCl4 group were recorded. Supplementation with chokeberry extract without CCl4 caused hyperproteinemia and hyperalbuminemia. Although the results indicate a weak protective role for AM, it is nevertheless important for improved erythropoiesis and regulation of the development of anemia. The hepatoprotective role of AM was moderate, and the immune response was not proven. Daily consumption of chokeberry extract can improve health. However, the results of our study showed that the ingestion of AM extract at this dose with the highest AOA would have more effective effects if the supplementation were significantly increased.

Vanadium(IV) complexes of salicylaldehyde-based furoic acid hydrazones: Synthesis, BSA binding and in vivo antidiabetic potential.

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.

Low-dose and repeated exposure to nickel leads to bioaccumulation and cellular and metabolic alterations in quails.

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.

L-cysteine protective effects against platelet disaggregation and echinocyte occurrence in gentamicin-induced kidney injury.

Gentamicin (GM) is an aminoglycoside antibiotic that induces nephrotoxicity. GM also causes necrosis of cells in the renal proximal tubules, resulting in acute tubular necrosis, followed by acute renal failure. Morphological alteration of blood cells, leukocytes and platelets count, as well as biochemical effects of L-cysteine (Cys) and antibiotic gentamicin, in clinically healthy male Wistar rats, were studied. Rats were divided into four groups: control (injected with 0.9% saline i.p.), GM (80 mg/kg b.w.; gentamicin injected i.p.), Cys-GM (100 mg/kg b.w.; L-cysteine and 80 mg/kg b.w. gentamicin injected i.p.), and Cys-GM-Cys (administered double dosage of 100 mg/kg b.w. L-cysteine and 80 mg/kg b.w. gentamicin i.p.). Biochemical and hematological analyses were performed on blood samples taken six days after treatments. Total proteins, albumin concentration and A/G ratio were significantly lower in experimental groups. Cholesterol, triglycerides, urea, and creatinine concentrations were significantly higher in relation to control. GM-induced lymphocytopenia, thrombocytopenia and neutrophilia. Echinocytosis and platelet disaggregation were found in all GM-treated animals. GM caused renal injury which indirectly led to erythrocyte abnormalities, changes in platelet aggregation, decreased protein fractions, and increased lipid and nitrogen components. The results suggest that GM-induced renal injury leads to significant biochemical changes in blood plasma, erythrocyte membrane impairment which can consequently cause anemia. Therefore, Cys might represent a novel therapeutic tool in the prevention and treatment of gentamicin-induced renal injury and blood cell disorders.

Ameliorative Effects of Propolis and Royal Jelly against CCl4 -Induced Hepatotoxicity and Nephrotoxicity in Wistar Rats.

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 .

Protective role of the dandelion extract against the blood-liver axis, cell membranes, and anemia disorder in sodium benzoate-exposed rats.

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.

Protective role of antithrombin III in suppressing acute responses in a rat model of renal ischemia-reperfusion injury.

Renal ischemia-reperfusion (IR) produces-induced injury and is characterized by restriction of blood supply to the kidney followed by restoration and re-oxygenation of the tissue. IR injury in the kidney contributes to pathological processes known as acute renal injury (ARI). Ischemia-perfusion injury (IRI) of the left renal artery has been demonstrated in Wistar rats. A total of 32 animals were divided into four groups: control group (SHAM), IR animals with induced ischemia-reperfusion, AT-IR animals treated by antithrombin III (AT) before IR, and AT-IR-AT animals with AT administered before and after IR. IR-induced hyperproteinemia, hyperalbuminemia, hyperglobulinemia, and a significantly low A/G ratio. Exogenous administration of AT prior to IR development effectively regulates protein fraction levels by establishing normoproteinemia. The preventive effect of AT regulates serum protein levels and reduces acute inflammation by reducing globulin and establishing physiological levels of A/G ratios. The therapeutic effect of AT given after IR is not effective compared to AT administered before IR. Protein fractions can serve as an important predictive marker for the prognosis and duration of acute inflammation. Serum globulin levels and the A/G ratio may serve as effective prognostic markers in acute inflammation caused by ischemia-reperfusion injury of the kidney. A strong correlation between globulin and the A/G ratio suggests novel markers associated with acute inflammation that can lead to chronic kidney disease.

Different outcomes of methadone maintenance therapy in rehabilitated and relapsed drug addicts: significance of liver and renal biomarkers.

Methadone eliminates heroin use, reduces death rates and criminality associated with heroin use, and improves patients' health and social productivity. This study included long-term addicts who completed a methadone therapy program as well as relapsed patients. Liver and renal markers important for methadone metabolism were analyzed. Renal markers included urea and creatinine, while hepatic markers included total bilirubin, AST, ALT, γGT, and LDH as nonspecific but significant parameters of liver metabolism. The study included 34 male and 6 female heroin-dependent patients undergoing a rehabilitation program with methadone maintenance treatment (MMT). During therapy, average values ​​of all parameters remained within the reference interval but individual parameters in some patients were very high. Significant differences for urea (0.00) and very high individual variations in all parameters, especially γGT and LDH, were found in patients who were in relapse. Age of the patients did not show a correlation with the presence of significant differences in serum biochemical parameters during therapy. Prolonged use of methadone therapy stabilizes high variations of liver and renal markers. MMT achieves a stabilization of serum indicators relevant for methadone metabolism that correlates with the duration of consumption and the type of opioid substance. The most important hepato-renal markers as indicators of therapy success are γGT, LDH, and creatinine. The validity of former enzymatic tests (AST, ALP, and ALT) should be seriously reconsidered in terms of MTT treatment success and monitoring the health of heroin addicts.

Evaluating the effects of anticoagulant rodenticide bromadiolone in Wistar rats co-exposed to vitamin K: impact on blood-liver axis and brain oxidative status.

The aim of this study was to investigate the beneficial effects of vitamin K relate to protection against detrimental effects of bromadiolone. Wistar rats (n = 30) were divided in three groups (n = 10): control group and two groups treated with bromadiolone (0.12 mg/kg) and bromadiolone + vitamin K (0.12 mg/kg + 100 mg/kg) over the period of four days. The main findings in the bromadiolone-exposed rats, such as damaged hepatocytes, high levels of globulin, total proteins and lymphocytes, and altered albumin/globulin ratio, collectively indicate an acute inflammatory process. Morphological changes in erythrocytes include microcytosis, hypochromia, hyperchromia, hemolysis, stomatocytosis, and spherocytosis. Significantly low values of RBC, Hct, and hemoglobin concentrations indicate impairments of the hematopoietic pathway causing combined anemia. The selected dose of bromadiolone caused a non-significant increase of catalase activity and a significant increase of the total protein content in brain tissue homogenates. Vitamin K supplementation reduced many of the harmful effects of bromadiolone. The cytoprotective role of vitamin K was proved to be of great importance for the preservation of structural changes on the membranes of hepatocytes and erythrocytes, in addition to the known role in the treatment of coagulopathies. The results of the study suggest valuable properties of vitamin K in the prevention and treatment of various types of anemia caused by bromadiolone toxicity. Future research is necessary to determine the adequate dose and treatment duration with vitamin K in disorders caused by the cumulative action of bromadiolone and possibly other pesticides.

Vitamin D3 attenuates oxidative stress and regulates glucose level and leukocyte count in a semi-chronic streptozotocin-induced diabetes model.

PURPOSE: Vitamin D3 (vit-D3) is a potent immunomodulator with anti-inflammatory and antioxidative properties. We used streptozotocin (STZ)-induced rat model of diabetes (DM) to evaluate the effects of vit-D3. We measured serum biochemical parameters, interleukin-17 (IL-17), osteocalcin (OC), malondialdehyde (MDA), and immune cell count on the 21st day of experiment. METHOD: A total of 24 Wistar rats were randomly divided into three groups. Each group had eight rats. During the 1st day of the experiment, the control group was injected intraperitoneally with citrate buffer, while STZ group and STZ + vit-D3 group were injected by a single i.p. dose (35 mg/kg) of STZ dissolved in citrate buffer (pH 4,5; 0,1 M). Vitamin D3 was applied via oral gavage once daily to the STZ + vit-D3 group for a total period of 14 days, starting from the 7th day of the experiment. RESULTS: STZ rats showed a significant reduction in OC and an increase in MDA and IL-17 serum concentrations compared to the control rats. We also observed a significant STZ-associated decrease in the number of lymphocytes and a significant increase in monocyte and eosinophil number. Oral treatment with vit-D3 to STZ-induced diabetic rats significantly increased OC and decreased MDA serum levels. Furthermore, vit-D3 treatment resulted in a good regulation of hematopoiesis such as increase in the number of segmented granulocytes and lymphocytes and a reduction in the number of monocytes and eosinophils. CONCLUSION: Vit-D3 treatment has important therapeutic effects; among many others it can attenuate oxidative stress and ameliorate the hyperglycemic state in the STZ-induced rat diabetic model, which is promising for further clinical trials.

Assessing hexavalent chromium tissue-specific accumulation patterns and induced physiological responses to probe chromium toxicity in Coturnix japonica quail.

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.

Lead Exposure Influences Serum Biomarkers, Hepatocyte Survival, Bone Marrow Hematopoiesis, and the Reproductive Cycle in Japanese Quails.

Lead toxicity has been a hallmark issue of toxicology over the last decades. However, predictive and non-robust models did not provide complete data on low-dose lead interaction with the organism at different functional levels (e.g., blood-serum-liver-bone marrow-bursa fabricii-reproductive system axis). Japanese quails are an animal model with a strong immune system, making them suitable for the thorough assessment of in vivo chronic lead toxicity. In this study, we have exposed Japanese quails via water ingestion to 0.25 and 0.5 µg/mL lead(II) chloride (PbCl2) for 20 days and assessed blood cells, serum biomarkers, hepatocyte survival, bone marrow hematopoiesis, bursa fabricii, and lead accumulation in eggs. Blood cells passed through morphological alterations (loss and inversion of the erythrocyte nucleus, multiple erythrocyte and thrombocyte aggregation, lymphocyte degradation, and blast cell infiltration). In the serum, PbCl2 increased the activity of creatine kinase (CK) and lactate dehydrogenase (LDH); increased the level of cholesterol, sodium, creatinine, and urea; and reduced the level of proteins, triglycerides, chloride, potassium, calcium, and alkaline phosphatase (ALP) activity (P < 0.05). Liver tissue of the exposed animals exhibited apparent death of hepatocytes. In the bone marrow, macrophages and heterophils contained a vast number of the infiltrated/uptaken granules upon PbCl2 exposure. Ultimately, PbCl2 exposure elicited a series of events observed first in the blood and serum parameters and later translated to the hematopoietic centers.

Morpho-functional alterations in lymphocytes and erythrocytes of Japanese quail due to prolonged in vivo exposure to heavy metal complexes.

BACKGROUND: Lead and cadmium are significant environmental pollutants that cause pathophysiological responses in many organs. Heavy metal absorption into many tissues is very fast due to a pronounced affinity for metallothioneins. METHOD: Japanese quail were exposed to different concentrations of metals (cadmium 0.20 mg/L and lead 0.25 and 0.50 mg/L) for 20 days. Erythrocytes (normal and hemolyzed) and lymphocytes (normal and altered) were monitored in this study. The analysis observed the percentage of normal and altered cells, as well as erythrocyte surface area. Cell counts were analyzed using light microscopy, while surface area and cytological changes in cells and nuclei were analyzed using licensed software. RESULTS: Different concentrations of metals have caused erythrocyte hemolysis as well as structural and morphological alterations in lymphocytes. Destruction of cell and nucleus membrane, changes in cell size, erythrocyte denucleation and reduced erythrocyte surface area were observed. Cadmium has caused erythrocyte hemolysis (29.30 %) and lymphocyte damage (92.10 %). Higher doses of lead resulted in greater damage to lymphocytes (63 %). Also, treatment with higher dose of lead produced a higher percentage of hemolyzed erythrocytes (19.20 %) in comparison to lower dose (9.90 %). CONCLUSION: The toxicity of heavy metals leads to reduced maturation of the blast, which causes the appearance of immature cells in peripheral circulation and severe destruction of blood cell membranes. Erythrocyte hemolysis can lead to anemia, while lymphocyte damage can lead to lymphocytopenia.

Chronic cadmium exposure in Japanese quails perturbs serum biochemical parameters and enzyme activity.

Cadmium is a heavy metal, toxic even in trace amounts and its biological function in the human body has not been described to date. It is assumed that cadmium manifests in dose-dependent genotoxic and cytotoxic effects on many organs and tissue types. In this study, we have analyzed the biochemical parameters in the serum of Japanese quails (Coturnix japonica) after chronic in vivo exposure to cadmium. Adult animals were exposed to cadmium in the form of CdCl2 dissolved in water (0.20 mg/L) for 20 days. Significant differences between controls and exposed animals were found in 12 out of 13 analyzed biochemical parameters. Total bilirubin concentrations did not show any significant differences between the two groups. Exposure to cadmium has resulted in a significant increase in lactate dehydrogenase activity, sodium and chloride concentration, as well as significant reductions in total proteins, albumins, globulins, glucose, triglycerides, cholesterol, calcium concentration, and alkaline phosphatase activity. In this sense, chronic in vivo exposure to low doses of cadmium has induced severe changes in the levels of observed biochemical parameters and enzyme activity. Additionally, evident cytogenetic changes in the liver were also noted, where hepatocyte damage and even lack of organized nuclei, including nuclear fragmentation, clearly indicated ongoing apoptotic processes.

Impairments of bone marrow hematopoietic cells followed by the sever erythrocyte damage and necrotic liver as the outcome of chronic in vivo exposure to cadmium: novel insights from quails.

Cadmium is a heavy metal classified as an environmental hazard, and its toxicity is subject to extensive research. Japanese quails were exposed to cadmium chloride (CdCl2) ad libitum for 20 days. Bone marrow, peripheral blood and liver were analyzed following the exposure. Moreover, we have provided the very first explanation of hematopoietic lines in Japanese quail. Following CdCl2 exposure, changes in the number, size and morphology of blood cells were observed in both peripheral blood and bone marrow. Alterations included severe erythrocyte damage, monocytosis and lymphopenia. In the liver of Cd-exposed animals we observed necrotic cells, absence of hematopoietic regions and cytogenetic changes of hepatocytes. Alterations in the bone marrow were also noted, as well as giant phagocytic cells, most likely macrophages. In vivo, CdCl2 exposure caused swift and destructive changes in the hematopoietic niche, liver and other tissues responsible for the detoxification cycle of cadmium and its compounds.