Effects of Combined Exposure to Aluminium and Ethanol on Aluminium Body Burden and some Neuronal, Hepatic and Haematopoietic Biochemical Variables in the Rat

Flora, S.J.S.; Dhawan, Mamta; Tandon, S. K.

doi:10.1177/096032719101000108

Cited by 25 publications

(9 citation statements)

References 20 publications

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“…It has been observed that combined exposure of aluminium and ethanol produced a more pronounced inhibition of hepatic alanine aminotransferase activity than either aluminium or ethanol alone (9). However, in the present investigation, ALT activity remained unaltered.…”

Section: Ethanol and Biochemical Changes Of Braincontrasting

confidence: 71%

“…This study suggested that, the ethanol exposure facilitate the aluminum accumulation in brain. Flora et al (9) Groups exposed to different treatment Normal Aluminum Ethanol Al & EtOH micro moles/100mg wet tissue aluminium and ethanol than in those exposed to aluminium alone.…”

Section: Resultsmentioning

confidence: 99%

“…Favarato and Zatta (23) also did not notice any alteration in serum AST activity in response to aluminum. Flora et al (9) observed that simultaneous exposure to aluminium and ethanol produced a significant elevation serum AST when compared to rats given aluminium alone. However, in the present investigation, aluminum exposure caused decrease in AST activity 'With ethanol' (23%) groups, with respect to its control group (Table 1).…”

Section: Ethanol and Biochemical Changes Of Brainmentioning

confidence: 99%

“…Davis (8) also hypothesized that the slowly progressive accumulation of aluminum in the brain, so as to reach functionally toxic levels, may be one of the factors to induce alcoholic amnesia or dementia. On the other hand, consumption of alcohol is suggested to increase susceptibility of rats to certain effects of aluminium (9). Hence the present study was undertaken to evaluate whether aluminum-induced general toxicity in brain is being potentiated by the simultaneous exposure to alcohol.…”

Section: Introductionmentioning

confidence: 99%

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Role of ethanol on aluminum induced biochemical changes on rat brain

Nayak

Das

Vasudevan

2006

Indian J Clin Biochem

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Section: Ethanol and Biochemical Changes Of Braincontrasting

confidence: 71%

Section: Resultsmentioning

confidence: 99%

Section: Ethanol and Biochemical Changes Of Brainmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Role of ethanol on aluminum induced biochemical changes on rat brain

Nayak

Das

Vasudevan

2006

Indian J Clin Biochem

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“…As with lead, simultaneous exposure to aluminium and ethanol also deplete brain dopamine (DA) and 5-hydroxytryptamine (5-HT) levels, when compared to rats given aluminium alone (Flora et al, 1991). Also, the concentration of aluminium in the blood and liver was significantly higher in rats exposed to both aluminium and ethanol than in those exposed only to aluminium.…”

Section: Environmental Neurotoxicants and Ethanol Intakementioning

confidence: 99%

Interaction Between Exposure to Neurotoxicants and Drug Abuse

Carvajal¹,

Sanchez-Amate²,

Lerma-Cabrera³

et al. 2012

Environmental Health - Emerging Issues and Practice

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Aluminium and the risk for alzheimer's disease

McLachlan

1995

Environmetrics

190

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SUMMARYThe strength of the evidence implicating aluminium as an important factor in the dementia of Alzheimer's disease (AD) is reviewed. We submit that the weight of the epidemiological and biological arguments is considerable. While a complete understanding has not been achieved, we recommend lowering aluminium exposure in municipal drinking water to below 50 pg/l in at least the province of Ontario. The Ministry of Energy and the Environment of Ontario maintains a drinking water surveillance programme which has provided a database for more than 10 years. This database has permitted assessment of the relative risk for AD using four independent measures of disease prevalence: 1. weighted residential history as a measure of exposure in autopsy-verified AD cases and controls; 2. first admission hospital discharge diagnoses of AD and controls; 3. death certificate rates for AD and presenile dementia; 4. impairments in cognitive function in elderly males. Taken together, many of the criticisms applied to epidemiological studies conducted elsewhere and reaching similar conclusions have been met. A vast experimental database on aluminium neurotoxicity, rapid advances in the understanding of the molecular basis of AD, and comparison studies between human brains exposed to chronic low dose aluminium exposure secondary to renal failure and AD, lend strong biological support to the conclusions reached by the epidemiological studies. The factors initiating AD, how aluminium gains access to the brain in AD, and the relative contributions of food, pharmaceuticals and skin absorption, remain unknown. While a full understanding is not in hand, the devastating nature of the disease, the lack of an effective treatment or prevention and the high cost to the health care system, together with the human costs, weighed against the relative cost of moderately reducing drinking water aluminium concentration to reduce exposure indicate that action is both reasonable and timely. KEY WORDSAlzheimer's disease; aluminium ALZHEIMER'S DISEASE: THE PROBLEMAlzheimer's disease (AD) is a slowly progressive, lethal, brain disorder which affects memory and other cognitive functions. AD is the most common cause of senile dementia and the prevalence in the age group over 65 years has been estimated to range between 9 per cent' and 5-5 per cent.2 The onset of AD is uncommon under the age of 65 (presenile dementia), but no less tragic. About 10 per cent of all cases occur in families (known as familial Alzheimer's disease (FAD)) and are inherited as an autosomal dominant disorder.The AD degenerative process renders victims mentally incompetent with progressive loss of self-help skills. The prolonged clinical course of the disease over ten or more years results in a particularly heavy burden of care upon the next-of-kin, the community social support systems, and, eventially, chronic care institutions, where the terminal phase may last three or more years. The brain changes which distinguish AD from all other causes of senile dementia are loss of neurons...

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Effects of Combined Exposure to Aluminium and Ethanol on Aluminium Body Burden and some Neuronal, Hepatic and Haematopoietic Biochemical Variables in the Rat

Cited by 25 publications

References 20 publications

Role of ethanol on aluminum induced biochemical changes on rat brain

Role of ethanol on aluminum induced biochemical changes on rat brain

Interaction Between Exposure to Neurotoxicants and Drug Abuse

Aluminium and the risk for alzheimer's disease

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