Fluoride and aluminium disturb neuronal morphology, transport functions, cholinesterase, lysosomal and cell cycle activities

Akinrinade, Ibukun; Memudu, Adejoke Elizabeth; Ogundele, Olalekan Michael

doi:10.1016/j.pathophys.2015.03.001

Cited by 40 publications

(17 citation statements)

References 35 publications

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“…Increased activity of ALP indicates inflammation and neutrophil activation caused by Al in small intestine tissue. Akinrinade et al (2015) reported increased ALP activity in the brain due to Al treatment. Sumathi et al (2015) also found increased ALP activity in rat brain treated with Al.…”

Section: Discussionmentioning

confidence: 99%

Melatonin is a potent modulator of antioxidative defense and cellular proliferation against aluminum toxicity in rats

Bulan¹,

Sarikaya-Unal²,

Tunalı³

et al. 2015

Turk J Biol

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Section: Discussionmentioning

confidence: 99%

Melatonin is a potent modulator of antioxidative defense and cellular proliferation against aluminum toxicity in rats

Bulan¹,

Sarikaya-Unal²,

Tunalı³

et al. 2015

Turk J Biol

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“…Moreover, structure integrity is important in neuronal metabolism, and the structure damage is linked to some neurological disorders. Abnormal neurons have an adverse influence on spatial navigation in rats . In this study, we observed that Al damaged neuronal ultrastructure in hippocampus, including shrunk nucleus areas, condensed nuclear density, increased heterochromatin and expanded cytoplasmic vacuolar areas in the hippocampus of AlCl 3 ‐treated rats.…”

Section: Discussionmentioning

confidence: 56%

Effects of Aluminium on Long‐Term Memory in Rats and on SIRT1 Mediating the Transcription of CREB‐Dependent Gene in Hippocampus

Yan

Jin

Cao

et al. 2017

Basic Clin Pharma Tox

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Epidemiological investigations have shown that aluminium (Al) is an important neurotoxicant which can be absorbed by organisms via various routes. Previous studies have confirmed that exposure to Al could cause neurodegenerative diseases, decline CREB phosphorylation and then down-regulate the transcription and protein expression of its target genes including BDNF. However, recent studies revealed that CREB activation alone was far from enough to activate the expression of long-term memory (LTM)-related genes; there might be other regulatory factors involved in this process. Several studies showed that TORC1 might be involved in regulating the transcription of downstream target genes as well. Also, TORC1 could be mediated by SIRT1 during the formation of LTM. However, the role of CREB regulating system in Al-induced LTM impairment was still not utterly elucidated till now. This study was designed to establish the rat model of subchronic Al exposure to observe the neuroethology, regulatory factor levels and molecular biological alterations in hippocampal cells. The results showed that, with the increasing AlCl dose, blood Al content increased gradually; morphology of the hippocampus and neuronal ultrastructure were aberrant; in the Morris water maze test, the escape latency and distance travelled became longer, swimming traces turned more complicated in the place navigation test; intracellular Ca , cAMP levels declined significantly in AlCl -treated rats, followed by abated nuclear translocation of TORC1 and decreased SIRT1, TORC1 and pCREB levels. These results indicate that SIRT1 and TORC1 might play an important mediating role in Al-induced LTM impairment.

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“…These complexes may cross the blood brain barrier and accumulate in the brain thus inducing brain neurotoxicity. [69][70][71] Many other associations between increased fluoride concentrations in fluoridated drinking water and possible adverse effects were suggested, e.g., decreased total fertility rate in both females and males, 72 diabetes 73 and greater impairment of thyroid function. 74…”

Section: 2 Chronic Exposurementioning

confidence: 99%

Fluoride in Human Health and Nutrition

Štepec

Ponikvar‐Svet

2019

ACSi

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Fluorine is in the form of fluorides ubiquitous in nature and as such an inevitable part of our environment. In small amounts, it is known to have beneficial effects on dental health. On the other hand, excessive chronic intakes can result in adverse effects including the development of dental fluorosis in children and/or skeletal fluorosis in both children and adults. The adequate intake has been set, based on empirical observations, at 0.05 mg/day/kg body weight however, the threshold between beneficial and harmful effects is narrow. Despite numerous studies, knowledge on the fluoride toxicity is still relatively poor. In this review, the role and the effects of fluoride on human health are enlightened. Some of the fluoride controversies are discussed and future research directions suggested.

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Fluoride and aluminium disturb neuronal morphology, transport functions, cholinesterase, lysosomal and cell cycle activities

Cited by 40 publications

References 35 publications

Melatonin is a potent modulator of antioxidative defense and cellular proliferation against aluminum toxicity in rats

Melatonin is a potent modulator of antioxidative defense and cellular proliferation against aluminum toxicity in rats

Effects of Aluminium on Long‐Term Memory in Rats and on SIRT1 Mediating the Transcription of CREB‐Dependent Gene in Hippocampus

Fluoride in Human Health and Nutrition

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