Levels of arsenic, cadmium, lead, manganese and zinc in biological samples of paralysed steel mill workers with related to controls.
ABSTRACT The determination of essential trace and toxic elements in the biological samples of human beings is an important clinical screening procedure. This study aimed to assess the possible effects of environmental exposure on paralysed male workers (n = 75) belonging to the production and quality control departments of a steel mill. In this investigation, the concentrations of arsenic, cadmium, lead, manganese and zinc were determined in biological samples (blood, urine and scalp hair samples) of exposed paralysis and non-paralysed steel mill workers. For comparative purposes, unexposed healthy subjects of same age group were selected as referents. The elements in the biological samples were measured by atomic absorption spectrophotometry prior to microwave-assisted acid digestion. The validity of the methodology was checked by the biological certified reference materials. The results indicate that the level understudy elements in all three biological samples were significantly higher in paralysed workers of both groups (quality control and production) as compared to referents (p < 0.01). The possible connection of these elements with the aetiology of disease is discussed. The results also show the need for immediate improvements of workplace ventilation and industrial hygiene practices.
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ABSTRACT: Oxidant-mediated damage and the triggering of oxidant-sensitive transcription factors could be associated with the neurotoxic actions of aluminum, zinc and lead. Aluminum and lead could induce oxidative stress through their capacity to interact with active oxygen species, increasing their oxidant activity, or by affecting membrane rheology. Aluminum-membrane interactions can also affect signaling cascades. Zinc, at high and low concentrations, increases cell oxidant concentrations, affects AP-1 and NF-kappaB transcription factors and induces neuronal cell death. The capacity of lead to promote oxidative stress, affect cell signals and to induce cell death by apoptosis has been mostly attributed to its effect on different calcium-mediated cellular events. The mentioned mechanisms as well as the contribution of these metals to different neurodegenerative disorders are discussed.Molecular Aspects of Medicine 02/2004; 25(1-2):103-115. · 10.38 Impact Factor
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ABSTRACT: The pathogenesis of some heart diseases has been associated with changes in the balance of certain trace elements. We examined the association of iron, copper and zinc between biological samples (scalp hair, whole blood and urine) and mortality from myocardial infarction (MI) patients of (first, second and third heart attack). The biological samples were from 130 MI patients (77 male and 53 female, age range 45-60 years) and 61 healthy age-matched controls (33 male and 28 female). The metals in the biological samples were measured by the flame atomic absorption spectrophotometry, prior to microwave assisted acid digestion. The validity of the methodology was checked by the biological certified reference materials. During this study, 78% of the 32 patients aged >50 years, registered after the third MI attack died. In these subjects the concentration of Fe and Cu were increased by 0.83% and 3.12% in the scalp hair while in blood samples 9.7% and 22.5% were enhanced respectively, as compared to those who tolerated 3rd MI attack (p=0.072). The concentrations of Zn in whole blood and scalp hair samples were lower in MI patients as compared to normal subjects. Deficiency of zinc and high concentration of copper and iron may play a role in the development of heart disease.Clinica Chimica Acta 03/2008; 389(1-2):114-9. · 2.85 Impact Factor
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ABSTRACT: Amyotrophic lateral sclerosis (ALS) is a rapidly progressive, invariably lethal disease resulting from the premature death of motor neurons of the motor cortex, brainstem, and spinal cord. In approximately 15% of familial ALS cases, the copper/zinc superoxide dismutase gene is mutated; a juvenile form of familial ALS has been linked to chromosome 2. No cause has been identified in the remaining familial ALS cases or in sporadic cases and the selective neurodegenerative mechanism remains unknown. Deletions in 2 genes on chromosome 5q, SMN (survival motor neuron gene) and NAIP (neuronal apoptosis inhibitory protein gene), have been identified in spinal muscular atrophy, a disease also characterized by the loss of motor neurons. These genes are implicated in the regulation of apoptosis, a mechanism that may explain the cell loss found in the brains and spinal cords of patients with ALS. To determine whether the mutations causing neurodegeneration in spinal muscular atrophy are present in patients with ALS in whom the copper/zinc superoxide dismutase gene is not mutated. Patients in whom ALS was diagnosed were screened for mutations in the SMN and NAIP genes by single strand conformation analysis. We found 1 patient with an exon 7 deletion in the SMN gene; review of clinical status confirmed the molecular diagnosis of spinal muscular atrophy. No mutations were found in the remaining patients. The SMN and NAIP gene mutations are specific for spinal muscular atrophy and do not predispose individuals to ALS.JAMA Neurology 07/1999; 56(6):710-2. · 7.58 Impact Factor