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1 t to injury induced by excitotoxic stress or mitochondrial toxicity.
2 lar injury, acute interstitial nephritis, or mitochondrial toxicity.
3 oxic BH3 domain fails to support mutant SOD1 mitochondrial toxicity.
4 imal tubule seems particularly vulnerable to mitochondrial toxicity.
5 and cytoplasmic TK1) were used to study NRTI mitochondrial toxicity.
6 rylation by TK2 is integral to clinical NRTI mitochondrial toxicity.
7 AD) is a direct molecular link from Abeta to mitochondrial toxicity.
8 ugs cause unwelcome side-effects by inducing mitochondrial toxicity.
9 leolytic proofreading may also contribute to mitochondrial toxicity.
10 ble cytochrome P4501A1 against drug-mediated mitochondrial toxicity.
11 DNA polymerase (Pol gamma), causing unwanted mitochondrial toxicity.
12 action accounting for hGAPDH inhibition and mitochondrial toxicity.
13 he cellular response to oxidative stress and mitochondrial toxicity.
14 s the perturbation of Ca(2+) homeostasis and mitochondrial toxicity.
15 gated for oxo-nitrative stress and resultant mitochondrial toxicity after 48 hours by using flow cyto
17 nd clinical benefits, such as a reduction in mitochondrial toxicity and oxidative stress and an impro
18 eover, FIAU (50 microm) produced significant mitochondrial toxicity ( approximately 70% decrease in m
21 xide synthase inhibitor, are associated with mitochondrial toxicity, asthma, and metabolic syndrome.
22 NRTI phosphorylation seems to correlate with mitochondrial toxicity, but experimental evidence is lac
23 olymerase gamma (pol gamma), participates in mitochondrial toxicity by incorporating these chain-term
25 hENTs may explain the clinically significant mitochondrial toxicity caused by the anti-HIV nucleoside
27 arametric high-content screening (mp-HCS) of mitochondrial toxicity holds promise as a lead in-vitro
28 n lead to varying clinical manifestations of mitochondrial toxicity (i.e., neuropathy, myopathy, lact
30 gs followed by proofreading failure leads to mitochondrial toxicity in antiviral therapy, and misinco
31 f the hypoxia response is protective against mitochondrial toxicity in cultured cells and zebrafish m
32 be an alternative; however, even if no overt mitochondrial toxicity is detected, widespread changes i
35 e explanation for the dramatic difference in mitochondrial toxicity of FIAU between humans and rodent
38 photoirradiation significantly enhances the mitochondrial toxicity of MKT-077 at both the biochemica
39 mitochondrial DNA polymerase and its role in mitochondrial toxicity of nucleoside analogues used to t
40 mbrane and that this expression enhances the mitochondrial toxicity of nucleoside drugs such as FIAU.
42 mbrane and that this expression enhances the mitochondrial toxicity of the nucleoside drug, fialuridi
43 cisplatin, HgCl(2), and gentamicin exhibited mitochondrial toxicity prior to decreases in basal respi
44 fic target and active partner in mutant SOD1 mitochondrial toxicity suggests new therapeutic strategi
45 analogues that cause neuropathy exert direct mitochondrial toxicity that is not mediated indirectly t
46 ridine; FIAU) produce clinically significant mitochondrial toxicity that limits their dose or prevent
47 assay, subsequent screening of compounds for mitochondrial toxicity (uncoupling and inhibition), data
48 utation R964C, which predisposes patients to mitochondrial toxicity when receiving 2',3'-didehydro-2'
49 scuous viral thymidine kinase and otherwise, mitochondrial toxicity would accumulate during long term
50 bitors, combined with propranolol, can cause mitochondrial toxicity, yielding potential clues about t
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