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ADULT HIPPOCAMPAL NEURAL STEM/PROGENITOR CELLS IN VITRO ARE VULNERABLE

TO THE MYCOTOXIN OCHRATOXIN-A

<http://toxsci.oxfordjournals.org/cgi/content/abstract/98/1/187?

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e & fdate=1/1/2002 & resourcetype=HWCIT>

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http://etd.lib.ttu.edu/theses/available/etd-05252005-163223/

The mechanisms of neurotoxicity induced by a Stachybotrys chartarum

Trichothecene Mycotoxin in an in vitro model

Karunasena, Enusha

CHAPTER V

THE TOXOLOGICAL EFFECTS OF SATRATOXIN H

ON HUMAN PROGENITOR NEURAL CELLS

" Neurons develop from the same cells as neuroglia in the CNS [1]. However,

neurons and glial cells are distinguished by their physiology [1]. Neurons

have polarized extensions, such as the axon and dendrites [1]. In addition

these cells are able to propagate an action potential, corresponding with

other neurons with the use of neurotransmitters at synaptic junctions [1].

Glial cells and ependymal cells of the CNS do not have axons or dendrites

[1]. During neuroinflammation, neurons tend to be damaged by immune

responses and studies have demonstrated that the reaction of astrocytes and

endothelial cells amplify CNS damage [2].

Neural damage can lead to permanent physiological effects. Studies conducted

on students who were exposed to poor IAQ due to fungal contamination,

demonstrated acoustic mycotic neuroma. Initial symptoms associated with this

condition included sensorineural hearing loss, tinnitus, and unsteadiness

[3]. This condition is associated with hearing loss and tumor development in

nerve tissues associated with hearing and this tumorous tissue must be

removed through surgical techniques [3]. This syndrome is normally seen in

the elderly population, however in one study, adolescent students were found

to have high levels of this condition [3]. In addition, these individuals

had other symptoms associated with neurological damage from SBS conditions,

such as headaches, memory loss, and lack of concentration, fatigue, sleep

disturbance, facial swelling, rashes, nosebleeds, diarrhea, abdominal pains

and respiratory problems [4].

The purpose in evaluating neural cells was to determine if satratoxin H

would produce toxic events in these cells. Neural cells are unable to repair

extensive cellular damage in the event of cytotoxic events that induce

apoptosis or severe inflammatory events. Thus, the objective of these

experiments was to evaluate, if in the event that macrocyclic trichothecenes

such as satratoxin H were able to enter neural cells, the effects these

toxins would have on cellular homeostasis. The purpose of these experiments

was to determine if neural damage could be induced by macrocyclic

trichothecenes at the low-doses that may be present in SBS conditions. "

Continued in paper at:

http://etd.lib.ttu.edu/theses/available/etd-05252005-163223/unrestricted/Karunas\

ena_Enusha_Diss.pdf

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