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Nanocarriers with disulfide bonds can help carry out the redox reaction that oxidizes glutathione, which may increase cellular apoptosis [14].
Tanno et al [20] indicate that SIRT1 nucleocytoplasmic shuttling, in response to oxidative stress, is a regulatory mechanism which may increase cellular resistance to apoptosis.
Leukocyte activation may increase cellular resistance to membrane-active agents [ 38].
In turn estrogens may increase cellular IGF1 through crosstalk, and IGF1 may up-regulate the receptor response to estrogens[ 61].
In addition, burning Chinese incense releases polycyclic aromatic hydrocarbons (Lung et al. 2003), which may increase cellular oxidative stress (Wu et al. 2003).
On the other hand, Cu is essential for optimal antioxidant defense, and a Cu deficiency may increase cellular susceptibility to oxidative damage [ 21].
Similar(52)
Exercise and dietary energy restriction reduce HNE production and may also increase cellular systems for HNE detoxification including glutathione and oxidoreductases.
Reduced CPE expression may therefore increase cellular susceptibility to injury.
Stronger light sources and the use of vital dyes may also increase cellular light toxicity, however, through increased light exposure and phototoxicity [ 9].
While telomerase adds telomeric repeats de novo contributing to enhanced proliferative capacity and lifespan, it may also increase cellular survival by conferring resistance to apoptosis.
A common pathophysiologic effect of many tobacco smoke components may be to increase cellular oxidant stress, which can lead to altered host defense and virus clearance (Cho et al. 2009).
Related(20)
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