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J Clin Exp Tox 2017 | Volume 1 | Issue 2
Toxicology and Pharmacology
November 01-02, 2017 | Toronto, Canada
International Conference on
Endogenous negative regulators of inflammation preserve neuronal survival
Denis Gris
University of Sherbrooke, Canada
C
yanotoxins have been shown to be highly toxic for
mammalian cells, including brain cells. However, little is
known about their effect on inflammatory pathways. Our study
investigated whether mammalian brain and immune cells can
be a target of certain cyanotoxins, at doses approximating
those in the guideline levels for drinking water. We examined
the effects on cellular viability, apoptosis, and inflammation
signaling of several toxins on murine macrophage-like
RAW264.7, microglial BV-2, and neuroblastoma N2a cell lines.
We have tested cylindrospermopsin (CYN), microcystin-LR (MC-
LR), and anatoxin-a (ATXa), individually as well as in mixture.
Searching into protective mechanism against cyanotoxins,
we found that Nlrx1, a protein localized to mitochondria,
ameliorates toxin effects. Decreased expression of Nlrx1
correlated with increased vulnerability of all cell types to toxin
exposure. Our results demonstrate that CYN, MC-LR, and ATX-a,
at low doses individually and in mixture, have potent effect
inducing apoptosis and inflammation. Further research of
the neuroinflammatory effects of these compounds
in-vivo
is
needed to improve safety limit levels for cyanotoxins in drinking
water and food.
Speaker Biography
Denis Gris has completed his PhD in the Neuroscience program at the Western
University of Ontario and moved to the University of North Carolina at Chapel Hill
where he studied mechanism of immune responses. His laboratory studies a role of
inflammation in the development and progression of neurodegenerative disorders and
using
in-vitro
and
in-vivo
models, he aims to uncover novel endogenous pathways that
limit neuroinflammation. At his lab, with his co-workers, they pair molecular work with
latest state-of-the-art automated behavioral assessment technology, to study how
inflammation changes CNS function.
e:
Denis.Gris@usherbrooke.ca