Prognostic significance of low serum levels of Clara cell phospholipid-binding protein in occupational aluminium neurotoxicity

Hałatek, Tadeusz; Sińczuk-Walczak, H; Rydzyński, K

doi:10.1016/j.jinorgbio.2005.06.027

Cited by 17 publications

(7 citation statements)

References 40 publications

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“…The molecular features of the lung proteins and their exchangeable pool appear to be critical. Bearing all this in mind, it seems reasonable to believe that the aluminum indirectly interacts in the CC16 decrease via metal-related changes in the lipid matrix of the membrane [91][92][93][94][95]. In our study group (foundry department workers), only casting smelters showed Al-U levels significantly higher than in controls.…”

Section: Ijomeh 2006;19(4)mentioning

confidence: 55%

“…Our results and those of several other authors [43,96,100,101] show that an extensive study is needed to determine a more correct TLV and health-based permissible concentration for occupational exposure to Al. Changes in and adverse effects on the central nervous system, for example, which can be observed at levels below the actual German and Finnish BEI standard for Al-U concentration in Al welders should be taken into account [56,95]. Future studies on respiratory morbidity should explore the interaction of mixtures, which may show a synergistic activity.…”

Section: Ijomeh 2006;19(4)mentioning

confidence: 99%

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Serum Clara Cell Protein as an Indicator of Pulmonary Impairment in Occupational Exposure at Aluminum Foundry

Hałatek¹,

Trzcinka-Ochocka²,

Matczak³

et al. 2006

International Journal of Occupational Medicine and Environmental Health

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Objectives: Although some of the exposures in aluminum (Al) smelting have been well characterized, and respiratory disorders in aluminum production workers are well known, the relationship between internal aluminum loads and appropriate lung biomarkers have not been elucidated. The aim of our work was to carry out a comprehensive investigation in workers employed in the Aluminum Foundry Casting Department with special reference to currently existing hygiene standards, known as threshold limit values (TLV) based on aluminum effects on the respiratory system. The measurement of serum anti-inflammatory Clara cell protein (CC16) was employed as a peripheral marker of the lung epithelium function. Materials and Methods: A group of 50 casting smelters, 5 locksmiths, 11 sawyers and auxiliary workers exposed to dust containing 14% of aluminum, and a group of 42 controls were examined. Respiratory function tests were performed and forced volume capacity (FVC), forced expiratory volume in 1 s (FEV 1 ), forced expiratory volume in the first percent (FEV 1 %), forced expiratory flows in 50% VC (FEV 50 ), and markers of foundry workers' exposure and body burden, Al concentration in the breathing zone, blood and urine, biomarkers of the effects of exposure, concentration of CC16 and hyaluronic acid (HA) in serum were determined in all examined workers. Additional measurements comprised determinations of serum iron (Fe) levels, myeloperoxidase (MPO), eosinophil cationic protein (ECP), immunoglobulin E (IgE), glutathione S-transferase (GST), and superoxide dismutase (SOD) activity in erythrocytes. Results: The group of casting smelters was characterized by the highest levels of aluminum in urine (Al-U) (43.7 mg L -1 ), high levels of MPO, ECP and IgE, high SOD activity, low CC16 levels, and low activity of GST. Lower Al-U excretion was observed in locksmiths (35.2 mg L -1 ) and sawyers (21.7 mg L -1 ). Serum CC16 proved to be the most sensitive biomarker, showing high inverse relationship with serum Al (Al-S) concentrations in casting smelters (p = 0.006). Conclusions: The study showed that in conditions of occupational exposure, dusts containing Al 2 O 3 < 1 mg m -3 cause changes in the respiratory system and biomarkers in serum, especially in CC16, connected with altered functioning of this system. Changes in concentrations of the examined biomarkers and also in respiratory parameters of the study subjects were observed when Al-U concentration was > 40 mg L -1 .

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Section: Ijomeh 2006;19(4)mentioning

confidence: 55%

Section: Ijomeh 2006;19(4)mentioning

confidence: 99%

Serum Clara Cell Protein as an Indicator of Pulmonary Impairment in Occupational Exposure at Aluminum Foundry

Hałatek¹,

Trzcinka-Ochocka²,

Matczak³

et al. 2006

International Journal of Occupational Medicine and Environmental Health

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“…Although the physiological requirement for Al has yet to be defined, it has been posited that Al may have an etiopathogenic role in neurodegenerative diseases (Halatek et al, 2005). Studies with Al in the form of AlCl 3 , Al(NO 3 ) 3 , or Al 2 (SO 4 ) 3 identified phenotypic abnormalities, including toxic effects on lifespan, body size, development, reproduction, locomotion, behavioral plasticity, and memory in the worm (Wang et al, 2009; Page et al, 2012).…”

Section: Techniques For Studying Neurodegeneration In C Elegansmentioning

confidence: 99%

Metal-induced neurodegeneration in C. elegans

Chen¹,

Martinez-Finley²,

Bornhorst³

et al. 2013

Front. Aging Neurosci.

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The model species, Caenorhabditis elegans, has been used as a tool to probe for mechanisms underlying numerous neurodegenerative diseases. This use has been exploited to study neurodegeneration induced by metals. The allure of the nematode comes from the ease of genetic manipulation, the ability to fluorescently label neuronal subtypes, and the relative simplicity of the nervous system. Notably, C. elegans have approximately 60–80% of human genes and contain genes involved in metal homeostasis and transport, allowing for the study of metal-induced degeneration in the nematode. This review discusses methods to assess degeneration as well as outlines techniques for genetic manipulation and presents a comprehensive survey of the existing literature on metal-induced degeneration studies in the worm.

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“…4 Aluminum is a vital etiopathogenic agent responsible for the incidence of neurodegenerative disease. 5 The response of A549 cells after exposure to different nanoparticles showed that Al 2 O 3 NPs induce a minor cytotoxic effect compared to nanometric titanium dioxide and carbon nanotubes.…”

Section: Introductionmentioning

confidence: 99%

Nanoalumina induces apoptosis by impairing antioxidant enzyme systems in human hepatocarcinoma cells

Alarifi¹,

Ali²,

Alkahtani³

2015

IJN

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Alumina nanoparticles (Al 2 O 3 NPs) are gradually used in various areas, including nanomedicine, biosensors, and electronics. The current study aimed to explore the DNA damage and cytotoxicity due to Al 2 O 3 NPs on human hepatocarcinoma cells (HepG2). The MTT and neutral red uptake assays showed that Al 2 O 3 NPs induce significant cell death in a dose- and time-dependent manner. However, Al 2 O 3 NPs induced significant intracellular reactive oxygen species production and elevated lipid peroxidation and superoxide dismutase levels in the HepG2 cells. Al 2 O 3 NPs also induced significant decrease in reduced glutathione levels and increase caspase-3 activity in HepG2 cells. DNA fragmentation analysis using the alkaline single-cell gel electrophoresis showed that Al 2 O 3 NPs cause genotoxicity in dose- and time-dependent manner. However, they induce reactive oxygen species production and oxidative stress, leading to oxidative DNA damage, a probable mechanism of genotoxicity. This study warrants more careful assessment of Al 2 O 3 NPs before their industrial application.

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Prognostic significance of low serum levels of Clara cell phospholipid-binding protein in occupational aluminium neurotoxicity

Cited by 17 publications

References 40 publications

Serum Clara Cell Protein as an Indicator of Pulmonary Impairment in Occupational Exposure at Aluminum Foundry

Serum Clara Cell Protein as an Indicator of Pulmonary Impairment in Occupational Exposure at Aluminum Foundry

Metal-induced neurodegeneration in C. elegans

Nanoalumina induces apoptosis by impairing antioxidant enzyme systems in human hepatocarcinoma cells

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