Browsing by Author "Cirovic, Ana (57217293503)"

Abstract: Heavy metals (HM)in the environment have provoked global attention because of its deleterious effects. This study evaluated the protection offered by Zn or Se or both against HMM-induced alterations in the kidney. Male Sprague Dawley rats were distributed into 5 groups of 7 rats each. Group I served as normal control with unrestricted access to food and water. Group II received Cd, Pb, and As (HMM) per oral daily for 60 days while groups III and IV received HMM in addition to Zn and Se respectively for 60 days. Group V received both Zn and Se in addition to HMM for 60 days. Metal accumulation in feces was assayed at days 0, 30, and 60 while accumulation in the kidney and kidney weight were measured at day 60. Kidney function tests, NO, MDA, SOD, catalase, GSH, GPx, NO, IL-6, NF-Κb, TNFα, caspase 3, and histology were assessed. There is a significant increase in urea, creatinine, and bicarbonate ions while potassium ions decreased. There was significant increase in renal function biomarkers, MDA, NO, NF-Κb, TNFα, caspase 3, and IL-6 while SOD, catalase, GSH, and GPx decrease. Administration of HMM distorted the integrity of the rat kidney, and co-treatment with Zn or Se or both offered reasonable protection suggesting that Zn or Se could be used as an antidot against the deleterious effects of these metals. Graphical Abstract: [Figure not available: see fulltext.]. © 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Abstract: Heavy metals (HM)in the environment have provoked global attention because of its deleterious effects. This study evaluated the protection offered by Zn or Se or both against HMM-induced alterations in the kidney. Male Sprague Dawley rats were distributed into 5 groups of 7 rats each. Group I served as normal control with unrestricted access to food and water. Group II received Cd, Pb, and As (HMM) per oral daily for 60 days while groups III and IV received HMM in addition to Zn and Se respectively for 60 days. Group V received both Zn and Se in addition to HMM for 60 days. Metal accumulation in feces was assayed at days 0, 30, and 60 while accumulation in the kidney and kidney weight were measured at day 60. Kidney function tests, NO, MDA, SOD, catalase, GSH, GPx, NO, IL-6, NF-Κb, TNFα, caspase 3, and histology were assessed. There is a significant increase in urea, creatinine, and bicarbonate ions while potassium ions decreased. There was significant increase in renal function biomarkers, MDA, NO, NF-Κb, TNFα, caspase 3, and IL-6 while SOD, catalase, GSH, and GPx decrease. Administration of HMM distorted the integrity of the rat kidney, and co-treatment with Zn or Se or both offered reasonable protection suggesting that Zn or Se could be used as an antidot against the deleterious effects of these metals. Graphical Abstract: [Figure not available: see fulltext.]. © 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

In the original version of this article, the affiliation 1 is incorrect. It is supposed to be “African Center of Excellence for Public Health and Toxicological Research (ACE-PUTOR), University of Port Harcourt, Nigeria”. The original article has been corrected. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024.

In the original version of this article, the affiliation 1 is incorrect. It is supposed to be “African Center of Excellence for Public Health and Toxicological Research (ACE-PUTOR), University of Port Harcourt, Nigeria”. The original article has been corrected. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024.

The tolerable aluminum (Al) intake levels for humans are constantly under review by regulatory agencies due to novel pre-clinical evidence on the neurotoxicity of prolonged Al exposure; however, little is known about the effects of Al on the spinal cord. This study aimed to investigate potential adverse effects on both spinal cord and systemic biochemical balance after prolonged exposure to a low dose of Al. Twenty adult rats were distributed in the control (distilled water) and exposed group (8.3 mg of AlCl3/kg/day). After 60 days, both blood and spinal cord samples were collected for oxidative stress and proteomic analyses. In plasma and erythrocytes, glutathione level was not different between groups; however, exposure to AlCl3 significantly decreased glutathione level in the spinal cord. Thiobarbituric acid reactive substances levels in the plasma and spinal cord of animals from the control group were significantly lower than those animals exposed to AlCl3. Exposure to AlCl3 significantly modulated the expression of proteins associated with the cell cycle, stimulus-response, cytoskeleton, nervous system regulation, protein activity, and synaptic signaling. Therefore, prolonged exposure to a low dose of Al triggered oxidative stress and proteomic changes that may affect spinal cord homeostasis. © 2022

The tolerable aluminum (Al) intake levels for humans are constantly under review by regulatory agencies due to novel pre-clinical evidence on the neurotoxicity of prolonged Al exposure; however, little is known about the effects of Al on the spinal cord. This study aimed to investigate potential adverse effects on both spinal cord and systemic biochemical balance after prolonged exposure to a low dose of Al. Twenty adult rats were distributed in the control (distilled water) and exposed group (8.3 mg of AlCl3/kg/day). After 60 days, both blood and spinal cord samples were collected for oxidative stress and proteomic analyses. In plasma and erythrocytes, glutathione level was not different between groups; however, exposure to AlCl3 significantly decreased glutathione level in the spinal cord. Thiobarbituric acid reactive substances levels in the plasma and spinal cord of animals from the control group were significantly lower than those animals exposed to AlCl3. Exposure to AlCl3 significantly modulated the expression of proteins associated with the cell cycle, stimulus-response, cytoskeleton, nervous system regulation, protein activity, and synaptic signaling. Therefore, prolonged exposure to a low dose of Al triggered oxidative stress and proteomic changes that may affect spinal cord homeostasis. © 2022

This study aimed to identify the landscape of current aluminum toxicity based on knowledge mapping of the 100 most-cited articles on toxicological aspects of aluminum in biological organisms. The research was searched in the Web of Science Core Collection (WoS-CC) with publications between 1945 and 2022. Data regarding authorship, title, journal, year of publication, citation count, country, keywords, study design, and research hotspots were extracted and all elected articles were analyzed. Our results showed that among the articles selected, literature review and in vivo studies were the most common study designs. The USA and England were found as the countries with most publications. Alzheimer’s disease (AD), aluminum, and neurotoxicity were found as the most frequent keywords. The articles most cited in world literature suggested that aluminum exposure is associated with Alzheimer’s disease, Parkinson’s disease (PD), dialysis encephalopathy, amyotrophic lateral sclerosis, neurodegeneration changes, cognitive impairment, such as bone damage, oxidative alterations, and cytotoxicity. © 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

This study aimed to identify the landscape of current aluminum toxicity based on knowledge mapping of the 100 most-cited articles on toxicological aspects of aluminum in biological organisms. The research was searched in the Web of Science Core Collection (WoS-CC) with publications between 1945 and 2022. Data regarding authorship, title, journal, year of publication, citation count, country, keywords, study design, and research hotspots were extracted and all elected articles were analyzed. Our results showed that among the articles selected, literature review and in vivo studies were the most common study designs. The USA and England were found as the countries with most publications. Alzheimer’s disease (AD), aluminum, and neurotoxicity were found as the most frequent keywords. The articles most cited in world literature suggested that aluminum exposure is associated with Alzheimer’s disease, Parkinson’s disease (PD), dialysis encephalopathy, amyotrophic lateral sclerosis, neurodegeneration changes, cognitive impairment, such as bone damage, oxidative alterations, and cytotoxicity. © 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

The preventability of acute lymphocytic leukemia during childhood is currently receiving great attention, as it is one of the most common cancers in children. Among the known risk factors so far are those affecting the development of gut microbiota, such as a short duration or absence of breastfeeding, cesarean section, a diet lacking in short-chain fatty acids (SCFAs), the use of antibiotics, absence of infection during infancy, and lack of pets, among other factors. Namely, it has been shown that iron deficiency anemia (IDA) and lack of vitamin D may cause intestinal dysbiosis, while at the same time, both increase the risk of hematological malignancies. The presence of IDA and vitamin D deficiency have been shown to lead to a decreased proportion of Firmicutes in stool, which could, as a consequence, lead to a deficit of butyrate. Moreover, children with IDA have increased blood concentrations of cadmium, which induces systemic inflammation and is linked to the onset of an inflammatory microenvironment in the bone marrow. Finally, IDA and Cd exposure increase fibroblast growth factor 23 (FGF23) blood levels, which in turn suppresses vitamin D synthesis. A lack of vitamin D has been associated with a higher risk of ALL onset. In brief, as presented in this review, there are three independent ways in which IDA increases the risk of acute lymphocytic leukemia (ALL) appearance. These are: intestinal dysbiosis, disruption of vitamin D synthesis, and an increased Cd load, which has been linked to systemic inflammation. All of the aforementioned factors could generate the appearance of a second mutation, such as ETV6/RUNX1 (TEL-AML), leading to mutation homozygosity and the onset of disease. ALL has been observed in both IDA and thalassemia. However, as IDA is the most common type of anemia and the majority of published data pertains to it, we will focus on IDA in this review. © 2024 by the authors.

[No abstract available]

Iron deficiency (ID) and iron deficiency anemia (IDA) have many adverse effects on human health. Also, iron deficiency anemia and anemia in general are linked with an increased risk of various cancers, particularly blood cancers. It is known that subjects with IDA as well as smokers have elevated blood levels of toxic divalent cations, particularly cadmium (Cd2+) and lead (Pb2+). Cadmium is a proven carcinogen. Most of the circulating cadmium is bound to transferrin and apart from the target organs of cadmium accumulation, kidney and liver, tissues (cells) which highly express transferrin receptor 1 (TfR1) may also accumulate high levels of circulating cadmium. Density of TfR1, glycoprotein that is expressed on cell surface, is not uniform in bone marrow cells. Namely, megakaryocyte/erythrocyte progenitors and pro-erythroblasts express TfR1 incomparably more than other cell lines within the bone marrow and we hypothesize that the mentioned cell lines will uptake most of the circulating cadmium and lead, and will consequently be most suitable for malignant transformation. In this review, we discuss in detail the mechanisms involved in accumulation of cadmium in particular cell lines of the bone marrow and the consequent occurrence of acute myeloid leukemia (AML). © 2021 Elsevier Ltd

Iron deficiency (ID) and iron deficiency anemia (IDA) have many adverse effects on human health. Also, iron deficiency anemia and anemia in general are linked with an increased risk of various cancers, particularly blood cancers. It is known that subjects with IDA as well as smokers have elevated blood levels of toxic divalent cations, particularly cadmium (Cd2+) and lead (Pb2+). Cadmium is a proven carcinogen. Most of the circulating cadmium is bound to transferrin and apart from the target organs of cadmium accumulation, kidney and liver, tissues (cells) which highly express transferrin receptor 1 (TfR1) may also accumulate high levels of circulating cadmium. Density of TfR1, glycoprotein that is expressed on cell surface, is not uniform in bone marrow cells. Namely, megakaryocyte/erythrocyte progenitors and pro-erythroblasts express TfR1 incomparably more than other cell lines within the bone marrow and we hypothesize that the mentioned cell lines will uptake most of the circulating cadmium and lead, and will consequently be most suitable for malignant transformation. In this review, we discuss in detail the mechanisms involved in accumulation of cadmium in particular cell lines of the bone marrow and the consequent occurrence of acute myeloid leukemia (AML). © 2021 Elsevier Ltd

[No abstract available]

[No abstract available]

[No abstract available]

Human environment is highly contaminated with aluminum, and aluminum is toxic to majority of tissues, particularly to neurons. In previous decades, aluminum exposure was frequently linked with the onset of Alzheimer’s disease (AD), and increased levels of Al were detected in the brains of individuals with AD. People who live in a certain area are exposed to aluminum in a similar way (they eat the same vegetable and other foodstuffs, use similar cosmetics, and buy medications from the same manufacturer), nevertheless not all of them develop Alzheimer’s disease. Majority of known risk factors for AD promote atherosclerosis and consequently reduce brain blood supply. In this review, we highlighted the significance of local (carotid disease and atherosclerosis of intracranial blood vessels) and systemic hypoxia (chronic obstructive pulmonary disease and anemia) in the development of AD. Nerve tissue is very sophisticated and sensitive to hypoxia and aluminum toxicity. As a side effect of compensatory mechanisms in case of hypoxia, neurons start to uptake aluminum and iron to a greater extent. This makes perfect a background for the gradual onset and development of AD. © 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Human environment is highly contaminated with aluminum, and aluminum is toxic to majority of tissues, particularly to neurons. In previous decades, aluminum exposure was frequently linked with the onset of Alzheimer’s disease (AD), and increased levels of Al were detected in the brains of individuals with AD. People who live in a certain area are exposed to aluminum in a similar way (they eat the same vegetable and other foodstuffs, use similar cosmetics, and buy medications from the same manufacturer), nevertheless not all of them develop Alzheimer’s disease. Majority of known risk factors for AD promote atherosclerosis and consequently reduce brain blood supply. In this review, we highlighted the significance of local (carotid disease and atherosclerosis of intracranial blood vessels) and systemic hypoxia (chronic obstructive pulmonary disease and anemia) in the development of AD. Nerve tissue is very sophisticated and sensitive to hypoxia and aluminum toxicity. As a side effect of compensatory mechanisms in case of hypoxia, neurons start to uptake aluminum and iron to a greater extent. This makes perfect a background for the gradual onset and development of AD. © 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Silica nanoparticles (SiNPs) have been touted for their role in the management of non-communicable diseases. Their neuroprotective benefits against heavy metal-induced neurotoxicity remain largely unexplored. This is a comparative evaluation of the oxido-inflammatory and neurotrophic effects of Ni, Al, and Ni/Al mixture on the cerebellum of male albino rats with or without treatment with SiNPs generated from melon seed husk. The study complied with the ARRIVE guidelines for reporting in vivo experiments. A total of 91, 7–9 week-old weight-matched male Sprague rats (to avoid sex bias) were randomly divided into 13 different dosing groups where Group 1 served as the control. Other groups received 0.2 mg/kg Ni, 1 mg/kg Al, and 0.2 mg/kg Ni + 1 mg/kg Al mixture with or without different doses of SiNP for 90 days. Rotarod performance was carried out. Oxidative stress markers, Ni, Al, Ca, Fe, Mg, neurotrophic factors, amyloid beta (Aβ-42), cyclooxygenase-2 (COX-2), and acetylcholinesterase (AChE) were determined in the cerebellum. SiNPs from melon seed husk caused a significant decrease in Aβ-42 level and activities of AChE and COX-2 and a significant increase in brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) mediated by Ni, Al, and Ni/Al mixture exposure in rats. Neurotoxicity of the Ni/Al mixture is via heightened neuronal lipoperoxidative damage, decreased Mg, and increased Fe, and co-administration of SiNPs from melon seed husk with the Ni/Al mixture attenuated some of these biochemical changes in the cerebellum. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. corrected publication 2024.

Silica nanoparticles (SiNPs) have been touted for their role in the management of non-communicable diseases. Their neuroprotective benefits against heavy metal-induced neurotoxicity remain largely unexplored. This is a comparative evaluation of the oxido-inflammatory and neurotrophic effects of Ni, Al, and Ni/Al mixture on the cerebellum of male albino rats with or without treatment with SiNPs generated from melon seed husk. The study complied with the ARRIVE guidelines for reporting in vivo experiments. A total of 91, 7–9 week-old weight-matched male Sprague rats (to avoid sex bias) were randomly divided into 13 different dosing groups where Group 1 served as the control. Other groups received 0.2 mg/kg Ni, 1 mg/kg Al, and 0.2 mg/kg Ni + 1 mg/kg Al mixture with or without different doses of SiNP for 90 days. Rotarod performance was carried out. Oxidative stress markers, Ni, Al, Ca, Fe, Mg, neurotrophic factors, amyloid beta (Aβ-42), cyclooxygenase-2 (COX-2), and acetylcholinesterase (AChE) were determined in the cerebellum. SiNPs from melon seed husk caused a significant decrease in Aβ-42 level and activities of AChE and COX-2 and a significant increase in brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) mediated by Ni, Al, and Ni/Al mixture exposure in rats. Neurotoxicity of the Ni/Al mixture is via heightened neuronal lipoperoxidative damage, decreased Mg, and increased Fe, and co-administration of SiNPs from melon seed husk with the Ni/Al mixture attenuated some of these biochemical changes in the cerebellum. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. corrected publication 2024.

We analyzed the bone microarchitecture of the subcapital and basicervical subregions of the femoral neck in men, to determine whether microarchitectural differences of cortical or trabecular bone can explain differential frequency of subcapital vs. basicervical fractures, especially in aged persons. The study sample encompassed twenty male proximal femora obtained during autopsy. They were divided in two age groups: young (< 40 years, n = 10) and aged (> 60 years, n = 10). Micro-computed tomography was used to evaluate cortical and trabecular microarchitecture of the subcapital and basicervical regions of the superolateral femoral neck–typical fracture initiation site. Basicervical region showed significantly thicker and less porous cortex than subcapital region (p = 0.02, p < 0.001, respectively), along with increased distance between cortical pores (p = 0.004) and smaller pore diameters (p = 0.069). Higher trabecular number (Tb.N: p = 0.042), lower trabecular thickness (Tb.Th: p < 0.001), and lower trabecular separation (p = 0.003) were also hallmarks of the basicervical compared to subcapital region, although BV/TV was similar in both regions (p = 0.133). Age-related deterioration was mostly visible in trabecular bone (for BV/TV, Tb.Th, Tb.N and fractal dimension: p = 0.026, p = 0.049, p = 0.059, p = 0.009, respectively). Moreover, there were tendencies to age-specific patterns of trabecular separation (more pronounced inter-site differences in aged) and cortical thickness (more pronounced inter-site differences in young). Trabecular microarchitecture corresponded to cortical characteristics of each region. Our study revealed the microarchitectural basis for higher incidence of subcapital than basicervical fractures of the femoral neck. This is essential for better understanding of the fracture risk, as well as for future strategies to prevent hip fractures and their complications. © 2020, Springer Science+Business Media, LLC, part of Springer Nature.