Non-thermal heat-shock response to microwaves

Pomerai, David de; Daniells, Clare; David, H. K.; Allan, Joanna; Duce, I.R.; Mutwakil, Mohammed H.A.Z.; Thomas, D.W.P.; Sewell, P.; Tattersall, J.E.H.; Jones, D.; Candido, P.

doi:10.1038/35013144

Cited by 190 publications

(161 citation statements)

References 8 publications

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“…Protein degradation is driven by the proteasome-dependent pathway through covalent binding of the target protein with ubiquitin, a 14 kDa small molecule [33,34]. HSPs act as molecular chaperones to prevent degradation of damaged proteins and remove them from the proteasome-dependent degrading pathway [15,16,41,42]. HSP90, the most abundant chaperone protein, is part of the multicomponent complex, and forms a superchaperone machine to promote the proper folding of client proteins.…”

Section: Discussionmentioning

confidence: 99%

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Chan

2007

Biochemical Journal

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The mycotoxin CTN (citrinin), a natural contaminant in foodstuffs and animal feeds, has cytotoxic and genotoxic effects on various mammalian cells. CTN is known to cause cell injury, including apoptosis, but the precise regulatory mechanisms of CTN action, particularly in stem cells and embryos, are currently unclear. In the present paper, I report that CTN has cytotoxic effects on mouse embryonic stem cells and blastocysts, and is associated with defects in their subsequent development, both in vitro and in vivo. Experiments in embryonic stem cells (ESC-B5) showed that CTN induces apoptosis via ROS (reactive oxygen species) generation, increased Bax/Bcl-2 ratio, loss of MMP (mitochondrial membrane potential), induction of cytochrome c release, and activation of caspase 3. In this model, CTN triggers cell death via inactivation of the HSP90 [a 90 kDa isoform of the HSP (heat-shock protein) family proteins]/multichaperone complex and subsequent degradation of Ras and Raf-1, further inhibiting anti-apoptotic processes, such as the Ras → ERK (extracellular-signal-regulated kinase) signal transduction pathway. In addition, CTN causes early developmental injury in mouse ESCs and blastocysts in vitro. Lastly, using an in vivo mouse model, I show that consumption of drinking water containing 10 µM CTN results in blastocyst apoptosis and early embryonic developmental injury. Collectively, these findings show for the first time that CTN induces ROS and mitochondria-dependent apoptotic processes, inhibits Ras → ERK survival signalling via inactivation of the HSP90/multichaperone complex, and causes developmental injury in vivo.

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Section: Discussionmentioning

confidence: 99%

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Chan

2007

Biochemical Journal

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“…The induction of hsp16-1::reporter expression by microwaves is strongly temperature-dependent, since this response is undetectable at 24C but increases steeply from 24.5 through 25.0 to 25.5C (de Pomerai et al, 2000a). Although there is a plateau of low-level expression at and above 25C in shielded controls, reporter gene activity does not increase steeply until the temperature exceeds 27C.…”

Section: Introductionmentioning

confidence: 98%

“…This was detected using transgenic strains carrying stress-inducible hsp16-1::reporter constructs (principally a lacZ reporter in strain PC72), in which heat-induced expression becomes apparent only at temperatures exceeding 27C (de Pomerai et al, 2000a). At exposure temperatures of 25-26C, PC72 worms are sensitive to a variety of exogenous stressors, including heavy metals, pesticides, anti-worm-surface antibodies, and microwaves (Power et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

A small temperature rise may contribute towards the apparent induction by microwaves of heat-shock gene expression in the nematodeCaenorhabditis Elegans

Dawe

Smith

Thomas

et al. 2006

Bioelectromagnetics

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“…Transcription is stimulated by both low frequency ($10-10 2 Hz) electric fields Blank, 1995) and magnetic fields (Goodman and Blank, 1998), as well as by high frequency radio/microwave fields ($10 12 Hz) (dePomerai et al, 2000;Leszczynski et al, 2002;Weisbrot et al, 2003). The high frequency fields are truly electromagnetic in that the electric and magnetic fields propagate together, whereas at low frequencies the fields can be effectively separated as alternating electric or magnetic fields.…”

mentioning

confidence: 99%

Initial interactions in electromagnetic field‐induced biosynthesis

Blank

Goodman

2004

Journal Cellular Physiology

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Low frequency electromagnetic (EM) fields induce gene expression, and recent insights into physical interactions of EM fields with model systems suggest a mechanism that could initiate this process. The consistently low thresholds at which EM fields stimulate biological processes indicate that they require little energy. Since it has been shown that such weak fields accelerate electron transfer reactions, they could stimulate transcription by interacting with electrons in DNA to destabilize the H-bonds holding the two DNA strands together. Such a mechanism is consistent with the low electron affinity of the bases in previously identified electromagnetic response elements (EMREs) needed for EM field interaction with DNA. It is also in line with both endogenous and in vitro stimulation of biosynthesis by electric fields. The frequency response of several EM sensitive biological systems suggests that EM fields require repetition and are most effective at frequencies that coincide with natural rhythms of the processes affected.

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Non-thermal heat-shock response to microwaves

Cited by 190 publications

References 8 publications

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

A small temperature rise may contribute towards the apparent induction by microwaves of heat-shock gene expression in the nematodeCaenorhabditis Elegans

Initial interactions in electromagnetic field‐induced biosynthesis

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