In vitro effect of aluminium upon erythrocyte membrane properties

Hernández, G.; Bollini, A; Huarte, M.; Bazzoni, Graciela; Piehl, Lidia Leonor; Chiarotto, Marcelo M; Celis, Emilio Rubín de; Rasia, M.

doi:10.3233/ch-2008-1129

Cited by 10 publications

(5 citation statements)

References 34 publications

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“…On the other hand, Al-induced polynuclear ions can also produce membrane changes and aggregate biomolecules (Flaten and Garruto, 1992). Again, chemicals such as Al induces the process of lipid peroxidation in the cell membrane (Hernandez et al, 2008), which is a principal cause of hepatotoxicity (Padi and Chopra, 2002). Lipid peroxidation is linked with the excess generation of reactive oxygen species (ROS), which may be contributed by the exogenous or the endogenous sources.…”

Section: Discussionmentioning

confidence: 99%

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The genotoxic, hepatotoxic, nephrotoxic, haematotoxic and histopathological effects in rats after aluminium chronic intoxication

et al. 2012

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Aluminium (Al) is used in water purification and is also present in several manufactured foods and medicines. Al is known to induce a broad range of physiological, biochemical and behavioural dysfunctions in laboratory animals and humans. This investigation was carried out to investigate the effects of subchronic exposure to Al (as AlCl3) in rats. Sprague-Dawley rats were randomly separated into two groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with Al (as AlCl3, 5 mg/kg body weight) intraperitonally for 10 weeks. Animals were killed and blood samples were analyzed for blood serum alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) enzyme activities and creatinine, urea (U) and uric acid (UA) levels for evaluating hepatotoxicity and nephrotoxicity. Blood parameters including red blood cells (RBCs), haemoglobin (Hb) concentration, haematocrit (Ht), platelets (PLTs) and white blood cells (WBCs) were compared between control and experimental group to assess haematoxicity. In order to determine the genotoxicity, the number of micronucleated hepatocytes (MNHEPs) was counted in isolated hepatocytes. In addition, histological alterations in liver and kidney samples were investigated. After exposure with Al, the enzymatic activities of ALP, AST, ALT and LDH, and the levels of U and UA significantly increased. RBC, WBC, PLT, Hb and Ht revealed significant decreases in experimental group compared to the control. AlCl3 caused a significant increase in MNHEPs. Furthermore, severe pathological damages were established in both liver and kidney samples. Subchronic exposure to low doses of Al can produce serious dysfunctions in rat blood, liver and kidney, and exposure to this metal can result in greater damages.

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Section: Discussionmentioning

confidence: 99%

“…One of the basic mechanisms of the toxic action of heavy metal on mammals is erythrocyte destruction (Mahieu et al, 2000). Hernandez et al (2008) reported the interaction of Al(III) with human RBC membrane. Erythrocyte life span was shortened because of the increased mechanical fragility of the cell membrane (Rao and Feldman, 1990).…”

Section: Discussionmentioning

confidence: 99%

The genotoxic, hepatotoxic, nephrotoxic, haematotoxic and histopathological effects in rats after aluminium chronic intoxication

et al. 2012

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“…Erythrocyte membrane permeability and osmotic fragility are affected by in vivo and in vitro Al exposures (Igbokwe, 2018). Erythrocyte osmotic fragility decreased (Bazzoni et al, 2005) or increased (Zatta et al, 1989;Hernández et al, 2008;Al-Qayim et al, 2014;Oztürk andOzdemir, 2015, Zhang et al, 2016;Cheng et al, 2018) depending on the Al speciation and type of erythrocyte injury. Eryptotic (apoptotic) injury reduces the erythrocyte aggregate size (Bazzoni et al, 2005) because of the shrinking effect, thereby increasing osmotic resistance (Igbokwe, 2016).…”

Section: Toxic Action or Effect Selected Referencesmentioning

confidence: 99%

“…Anemia caused by Al toxicity is not associated with adequate regenerative activity of the bone marrow and reticulocytosis (Chmielnicka et al, 1994;Osman et al, 2012). The additional causes of anemia appear to be multi-factorial and include defective hemoglobin production due to inhibition of the enzymes of heme synthesis, altered erythrocyte membrane structure and fragility, shortening of red blood cell life span due to eryptotic and oncotic injuries, and inadequate iron utilization (Zatta et al, 1989;Perez et al, 2001;Bazzoni et al, 2005;Vittori et al, 2002;Niemoeller et al, 2006;Hernández et al, 2008;Sadhana, 2011;Vota et al, 2012;Lukyanenko et al, 2013;Al-Qayim et al, 2014;Oztürk and Ozdemir, 2015;Zhang et al, 2016;Cheng et al, 2018). Significant decreases in hemoglobin, hematocrit (packed cell volume) and erythrocyte osmotic fragility were reported after Al exposure (Garbossa et al, 1996;Garbossa et al, 1998;Vittori et al, 1999;Farina et al, 2005).…”

Section: Hematologic Effectsmentioning

confidence: 99%

Aluminium toxicosis: a review of toxic actions and effects

Igbokwe

Igwenagu

Igbokwe

2019

Interdisciplinary Toxicology

229

149

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Aluminium (Al) is frequently accessible to animal and human populations to the extent that intoxications may occur. Intake of Al is by inhalation of aerosols or particles, ingestion of food, water and medicaments, skin contact, vaccination, dialysis and infusions. Toxic actions of Al induce oxidative stress, immunologic alterations, genotoxicity, pro-inflammatory effect, peptide denaturation or transformation, enzymatic dysfunction, metabolic derangement, amyloidogenesis, membrane perturbation, iron dyshomeostasis, apoptosis, necrosis and dysplasia. The pathological conditions associated with Al toxicosis are desquamative interstitial pneumonia, pulmonary alveolar proteinosis, granulomas, granulomatosis and fibrosis, toxic myocarditis, thrombosis and ischemic stroke, granulomatous enteritis, Crohn’s disease, inflammatory bowel diseases, anemia, Alzheimer’s disease, dementia, sclerosis, autism, macrophagic myofasciitis, osteomalacia, oligospermia and infertility, hepatorenal disease, breast cancer and cyst, pancreatitis, pancreatic necrosis and diabetes mellitus. The review provides a broad overview of Al toxicosis as a background for sustained investigations of the toxicology of Al compounds of public health importance.

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“…Additionally, Al(III) released by MMTs (Figure 3b) could also facilitate hole formation, because Al(III) could induce cell membrane damage by favoring lipid peroxidation reactions even at a relatively lower concentration (e.g., 0.027 mg/L). 52,53 Therefore, we hypothesize that hole formation in the E. coli cell membrane is highly plausible and would facilitate the entry of plasmid pUC19 into the cells, thus increasing the horizontal transfer of plasmid-borne ARGs. 49,54 Additionally, it is well-known that microorganisms could attach to soil clays.…”

Section: ■ Results and Discussionmentioning

confidence: 99%

Nonmonotonic Effect of Montmorillonites on the Horizontal Transfer of Antibiotic Resistance Genes to Bacteria

Sheng

Zhang

et al. 2020

Environ. Sci. Technol. Lett.

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Bacterial transformation is important to the transmission of antibiotic resistance genes (ARGs) in soils, and soil pore water is recognized as a hot spot for dissemination of ARGs. However, little is known about how concentrations and sizes of clay particles in soil pore water influence the horizontal transfer of ARGs. This study investigated the horizontal transfer of an antibiotic resistant plasmid (pUC19) into competent Escherichia coli cells with or without montmorillonites (MMTs, 0–2 g/L) with average sizes of 1568 nm (size-1500 fraction), 568 nm (size-500 fraction), and 300 nm (size-300 fraction). With increasing MMT concentrations, horizontal ARG transfer was initially enhanced and then became inhibited at transition concentrations of 0.100 g/L for the size-1500 fraction, 0.050 g/L for the size-500 fraction, and 0.025 g/L for the size-300 fraction. The smaller MMT size fractions had a stronger effect on horizontal ARG transfer. At lower MMT concentrations, horizontal ARG transfer was enhanced by an increased level of plasmid–cell contact and possible hole formation in the cell membrane, whereas at higher MMT concentrations, it was inhibited by binding of the plasmid to MMTs and its aggregation facilitated by released metal cations. Our results provided new insight into the influence of clay minerals on ARG transfer in soils, thus improving our understanding of the environmental fate of ARGs.

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In vitro effect of aluminium upon erythrocyte membrane properties

Cited by 10 publications

References 34 publications

The genotoxic, hepatotoxic, nephrotoxic, haematotoxic and histopathological effects in rats after aluminium chronic intoxication

The genotoxic, hepatotoxic, nephrotoxic, haematotoxic and histopathological effects in rats after aluminium chronic intoxication

Aluminium toxicosis: a review of toxic actions and effects

Nonmonotonic Effect of Montmorillonites on the Horizontal Transfer of Antibiotic Resistance Genes to Bacteria

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