Neurological syndromes produced by some toxic metals encountered industrially or environmentally

Bahiga,; Mahmoud, Lily H; Kotb, Nadia A.; El-Dessoukey, E. A.

doi:10.1007/bf02021115

Cited by 15 publications

(8 citation statements)

References 14 publications

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“…However, we cannot exclude the possibility that other structures within the zebrafish visual system are also altered by MeHg exposure, as has been shown in other preparations [30,57,58]. In fact, it is highly likely that these other regions are also sensitive and that it is the combined effect of MeHg exposure on various neural circuits that leads to the changes in visual behaviors observed.…”

Section: Discussionmentioning

confidence: 83%

“…Clearly, central nervous system integration with the optic tectum and/or cerebellum, altered function of the optic nerve, and/or sensorimotor deficiencies are all additional mechanisms that also could be involved. Lesions in brain regions important to visual discrimination, e.g., occipital lobe and striate cortex, after postnatal exposures to MeHg have been noted and have led to restricted peripheral vision [57,58]. In fishes, the optic tectum is the parallel brain region and it would not be unexpected to find structural and/or functional alterations there, as well.…”

Section: Discussionmentioning

confidence: 99%

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Selenomethionine reduces visual deficits due to developmental methylmercury exposures

Weber¹,

Connaughton²,

Dellinger³

et al. 2008

Physiology & Behavior

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Developmental exposures to methylmercury (MeHg) have life-long behavioral effects. Many micronutrients, including selenium, are involved in cellular defenses against oxidative stress and may reduce the severity of MeHg-induced deficits. Zebrafish embryos (<4 h post fertilization, hpf) were exposed to combinations of 0.0-0.30 microM MeHg and/or selenomethionine (SeMet) until 24 hpf then placed in clean medium. Fish were tested as adults under low light conditions ( approximately 60 microW/m(2)) for visual responses to a rotating black bar. Dose-dependent responses to MeHg exposure were evident (ANOVA, P<0.001) as evidenced by reduced responsiveness, whereas SeMet did not induce deficits except at 0.3 microM. Ratios of SeMet:MeHg of 1:1 or 1:3 resulted in responses that were indistinguishable from controls (ANOVA, P<0.001). No gross histopathologies were observed (H&E stain) in the retina or optic tectum at any MeHg concentration. Whole-cell, voltage-gated, depolarization-elicited outward K(+) currents of bipolar cells in intact retina of slices adult zebrafish were recorded and outward K(+) current amplitude was larger in bipolar cells of MeHg-treated fish. This was due to the intense response of cells expressing the delayed rectifying I(K) current; cells expressing the transient I(A) current displayed a slight trend for smaller amplitude among MeHg-treated fish. Developmental co-exposure to SeMet reduced but did not eliminate the increase in the MeHg-induced I(K) response, however, I(A) responses increased significantly over MeHg-treated fish to match control levels. Electrophysiological deficits parallel behavioral patterns in MeHg-treated fish, i.e., initial reactions to the rotating bar were followed by periods of inactivity and then a resumption of responses.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Selenomethionine reduces visual deficits due to developmental methylmercury exposures

Weber¹,

Connaughton²,

Dellinger³

et al. 2008

Physiology & Behavior

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“…Similarly, lead and alumin ium may be associated with the pathogenesis of certain forms of parkinsonism [ 17], Mer cury and manganese had also been reported to be associated with secondary parkinson ism [01, 15,18] but none of these have been etiologically associated with the idiopathic form.…”

Section: Discussionmentioning

confidence: 99%

“…Various other chemicals and metals, e.g. fluoroalkane solvent, carbon tetrachloride, lead and manganese, have been shown to cause a syndrome complex with parkinson ism albeit not the picture of classical idio pathic PD [14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Epidemiologic Study on the Association between Body Burden Mercury Level and Idiopathic Parkinson's Disease

Ngim¹,

Devathasan

1989

Neuroepidemiology

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A case-control study was conducted among the multiethnic population of Singapore to test the hypothesis that a high level of body burden mercury is associated with an increased risk of Parkinson''s disease (PD). Selected factors investigated that could contribute to the body burden of mercury included dietary fish intake, ethnic over-the-counter medications, occupational exposures and possession of dental amalgam fillings. Detailed interviews were completed in 54 cases of idiopathic PD and 95 hospital-based controls, matched for age, sex and ethnicity, between July 1985 and July 1987. After adjusting for potential confounding factors, including dietary fish intake, medications, smoking and alcohol consumption, there was clear monotonic dose-response association between PD and blood mercury levels. The odds ratios (OR) and 95% confidence intervals (CI) for the approximate subject tertiles based upon blood mercury levels were 8.5 (CI = 2.2–33.2) and 9.4 (CI = 2.5–35.9), relative to the tertile with lowest blood mercury levels (< 5.8 ng Hg/ml). Similar associations were revealed using scalp hair and urinary mercury levels. However, only the comparisons between the highest and lowest tertiles were statistically different from unity (p < 0.05). When the body burden mercury indicators were mutually adjusted in addition to the four confounding factors, blood and urinary mercury levels showed ORs of 21.00 and 18.65, respectively. These ORs were statistically different from unity (p < 0.05, 2-sided test). After adjustment, scalp hair mercury was shown to be a poor predictor of PD risk.

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“…The onset of arsenic neuropathy can be acute, as in arsenic poisoning or during treatment of APL with arsenic trioxide (Kühn, Sammartin, Nabergoj, & Vianello, 2016); chronic, as in environmental arsenic exposure; or acute-on-chronic, as in ORAI (Dani, 2013). The diagnosis of acute arsenic neuropathy is straightforward and based on the association of gastrointestinal disorders, encephalopathy and mood disorders (Bahiga, Kotb, & El-Dessoukey, 1978;Campbell & Alvarez, 1989;Ratnaike, 2003). Acute arsenic intoxication is strongly related to symmetrical peripheral neuropathy in the upper and lower limbs, so that the causal relation here is clear (Rodríguez, Jiménez-Capdeville, & Giordano, 2003;Vahidnia, van der Voet, & de Wolff, 2007).…”

Section: Arsenic Neuropathymentioning

confidence: 99%

Chronic arsenic intoxication diagnostic score (CAsIDS)

Dani

Walter

2017

J of Applied Toxicology

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Arsenic and its compounds are well-established, potent, environmentally widespread and persistent toxicants with metabolic, genotoxic, mutagenic, teratogenic, epigenetic and carcinogenic effects. Arsenic occurs naturally in the Earth's crust, but anthropogenic arsenic emissions have surmounted the emissions from important natural sources such as volcanism. Inorganic arsenicals exhibit acute and chronic toxicities in virtually all cell types and tissues, and hence arsenic intoxication affects multiple systems. Whereas acute arsenic intoxication is rare and relatively easy to diagnose, chronic arsenic intoxication (CAsI) is common but goes often misdiagnosed.Based on a review of the literature as well as our own clinical experience, we propose a chronic arsenic intoxication diagnostic score (CAsIDS). A distinctive feature of CAsIDS is the use of bone arsenic load as an essential criterion for the individual risk assessment of chronic arsenic intoxication, combined with a systemic clinical assessment. We present clinical examples where CAsIDS is applied for the diagnosis of CAsI, review the main topics of the toxicity of arsenic in different cell and organ systems and discuss the therapy and prevention of disease caused or aggravated by chronic arsenic intoxication. CAsIDS can help physicians establish the diagnosis of CAsI and associated conditions.

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Neurological syndromes produced by some toxic metals encountered industrially or environmentally

Cited by 15 publications

References 14 publications

Selenomethionine reduces visual deficits due to developmental methylmercury exposures

Selenomethionine reduces visual deficits due to developmental methylmercury exposures

Epidemiologic Study on the Association between Body Burden Mercury Level and Idiopathic Parkinson's Disease

Chronic arsenic intoxication diagnostic score (CAsIDS)

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