Showing posts with label Toxicity. Show all posts
Showing posts with label Toxicity. Show all posts

Monday, 25 September 2017

Dietary exposure and neurotoxicity of the environmental free and bound toxin β-N-methylamino-l-alanine

Food Research International, 100, 2017, Pages 1-13


The growing evidence supporting a link between exposure to the naturally occurring toxin β-N-methylamino-l-alanine (BMAA) and progressive neurodegenerative diseases, has recently arisen the interest of the scientific community. Latest investigations suggest that dietary exposure to this algal toxin may have been largely underestimated. This paper reviews the state of the art regarding BMAA, with special attention paid to its neurotoxicity, its concentration levels in food, and human exposure. As for other environmental toxins, dietary intake is most likely the main route of exposure to BMAA for the general population. However, data concerning BMAA levels in foodstuffs are still scarce. It is concluded that further investigations on dietary intake and potential human health effects are clearly necessary to assess the risks to public health associated with BMAA exposure. Some critical remarks and recommendations on future research in this area are provided, which may help to identify approaches to reduce dietary BMAA exposure.

Wednesday, 15 March 2017

Perspective on pre- and post-natal agro-food exposure to persistent organic pollutants and their effects on quality of life

Environment International


Background

Adipose tissue constitutes a continual source of internal exposure to organic pollutants (OPs). When fats mobilize during pregnancy and breastfeeding, OPs could affect foetal and neonatal development, respectively.

Scope and approach

The main aim of this review is to deal with pre- and post-natal external exposure to organic pollutants and their effects on health, proposing prevention measures to reduce their risk. The goal is the development of a biomonitoring framework program to estimate their impact on human health, and prevent exposure by recommending some changes in personal lifestyle habits.

Key findings and conclusions

It has been shown that new studies should be developed taking into account their cumulative effect and the factors affecting their body burden. In conclusion, several programs should continuously be developed by different health agencies to have a better understanding of the effect of these substances and to develop a unified public policy.

Friday, 12 June 2015

Toxicity evaluation of new agricultural fungicides in primary cultured cortical neurons

Environmental Research, 140, 2015, 37-44


Fungicides are crucial for food protection as well as for the production of crops of suitable quality and quantity to provide a viable economic return. Like other pesticides, fungicides are widely sprayed on agricultural land, especially in wine-growing areas, from where they can move-off after application. Furthermore, residues of these agrochemicals can remain on crops after harvest and even after some food processing operations, being a major exposure pathway. Although a relatively low toxicity has been claimed for this kind of compounds, information about their neurotoxicity is still scarce.

In the present study, nine fungicides recently approved for agricultural uses in the EU ― ametoctradin, boscalid, cyazofamid, dimethomorph, fenhexamid, kresoxim-methyl, mepanipyrim, metrafenone and pyraclostrobin ― have been evaluated for their toxicity in primary cultured mouse cortical neurons. Exposure to 0.1–100 µM for 7 days in vitro resulted in a dose-dependent toxicity in the MTT cell viability assay. Strobilurin fungicides kresoxim-methyl (KR) and pyraclostrobin (PY) were the most neurotoxic compounds (lethal concentration 50 were in the low micromolar and nanomolar levels, respectively) causing a rapid raise in intracellular calcium [Ca2+]i and strong depolarization of mitochondrial membrane potential. KR- and PY-induced cell death was reversed by the calcium channels blockers MK-801 and verapamil, suggesting that calcium entry through NMDA receptors and voltage-operated calcium channels are involved in KR- and PY-induced neurotoxicity. These results highlight the need for further evaluation of their neurotoxic effects in vivo.