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1  an HIV+ patient on tenofovir-based ART with mitochondrial toxicity.
2 DNA polymerase (Pol gamma), causing unwanted mitochondrial toxicity.
3  action accounting for hGAPDH inhibition and mitochondrial toxicity.
4 he cellular response to oxidative stress and mitochondrial toxicity.
5 s the perturbation of Ca(2+) homeostasis and mitochondrial toxicity.
6 t to injury induced by excitotoxic stress or mitochondrial toxicity.
7 lar injury, acute interstitial nephritis, or mitochondrial toxicity.
8 t PrimPol protects against tenofovir-induced mitochondrial toxicity.
9 oxic BH3 domain fails to support mutant SOD1 mitochondrial toxicity.
10 imal tubule seems particularly vulnerable to mitochondrial toxicity.
11 and cytoplasmic TK1) were used to study NRTI mitochondrial toxicity.
12 rylation by TK2 is integral to clinical NRTI mitochondrial toxicity.
13 AD) is a direct molecular link from Abeta to mitochondrial toxicity.
14 s and, therefore, a potential contributor to mitochondrial toxicity.
15 ugs cause unwelcome side-effects by inducing mitochondrial toxicity.
16 leolytic proofreading may also contribute to mitochondrial toxicity.
17 ble cytochrome P4501A1 against drug-mediated mitochondrial toxicity.
18 bunit protein that might make it relevant to mitochondrial toxicity.
19 ically phosphorylated tau reported to induce mitochondrial toxicity.
20 samples, was multiplexed with an endpoint of mitochondrial toxicity.
21 gated for oxo-nitrative stress and resultant mitochondrial toxicity after 48 hours by using flow cyto
22 hat citalopram reduces mutant APP and AB and mitochondrial toxicities and may have a protective role
23          We aimed to assess CPC's effects on mitochondrial toxicity and endocrine disruption in vitro
24 o Conversely, REST overexpression attenuated mitochondrial toxicity and mitochondrial morphology disr
25 nd clinical benefits, such as a reduction in mitochondrial toxicity and oxidative stress and an impro
26                                              Mitochondrial toxicity and the oxidative stress response
27 iotic metabolism, adaptive stress responses, mitochondrial toxicity, and neurotoxicity.
28  to be nongenotoxic, nonmutagenic, devoid of mitochondrial toxicity, and possessed no ion channel lia
29 eover, FIAU (50 microm) produced significant mitochondrial toxicity ( approximately 70% decrease in m
30                   However, the mechanisms of mitochondrial toxicity are still unclear.
31                        New evidence supports mitochondrial toxicity as a principal mechanism for dide
32                    We developed a cell-based mitochondrial toxicity assay for environmental chemicals
33 xide synthase inhibitor, are associated with mitochondrial toxicity, asthma, and metabolic syndrome.
34 NRTI phosphorylation seems to correlate with mitochondrial toxicity, but experimental evidence is lac
35 olymerase gamma (pol gamma), participates in mitochondrial toxicity by incorporating these chain-term
36                                              Mitochondrial toxicity can result from antiviral nucleot
37 hENTs may explain the clinically significant mitochondrial toxicity caused by the anti-HIV nucleoside
38 ver, the guanidines circumvent an off-target mitochondrial toxicity exhibited by the imidazoliums.
39                                              Mitochondrial toxicity has been purported as the major t
40 arametric high-content screening (mp-HCS) of mitochondrial toxicity holds promise as a lead in-vitro
41 n lead to varying clinical manifestations of mitochondrial toxicity (i.e., neuropathy, myopathy, lact
42  amyloid-beta and p-tau-induced synaptic and mitochondrial toxicities in AD.
43  ligand 1 against Abeta-induced synaptic and mitochondrial toxicities in mouse neuroblastoma (N2a) ce
44 ta is likely a direct link between Abeta and mitochondrial toxicity in Alzheimer's disease.
45 gs followed by proofreading failure leads to mitochondrial toxicity in antiviral therapy, and misinco
46 f the hypoxia response is protective against mitochondrial toxicity in cultured cells and zebrafish m
47                   TDF/FTC-based PrEP induces mitochondrial toxicity in healthy subjects after 12 mont
48 ew provides the basis for the involvement of mitochondrial toxicity in the different functional hallm
49 ncy virus infection, and their use can cause mitochondrial toxicity, including mitochondrial DNA (mtD
50 be an alternative; however, even if no overt mitochondrial toxicity is detected, widespread changes i
51                                              Mitochondrial toxicity is relatively low because acyclov
52                                              Mitochondrial toxicity limits nucleoside reverse transcr
53 development of ophthalmic diseases, elevated mitochondrial toxicity of antiviral drugs and increased
54 e explanation for the dramatic difference in mitochondrial toxicity of FIAU between humans and rodent
55            Our data suggest that the lack of mitochondrial toxicity of FIAU in mice is due to the lac
56                                          The mitochondrial toxicity of FIAU to Madin-Darby canine kid
57  photoirradiation significantly enhances the mitochondrial toxicity of MKT-077 at both the biochemica
58 mitochondrial DNA polymerase and its role in mitochondrial toxicity of nucleoside analogues used to t
59 mbrane and that this expression enhances the mitochondrial toxicity of nucleoside drugs such as FIAU.
60                          We investigated the mitochondrial toxicity of the lipophilic cation, MKT-077
61 mbrane and that this expression enhances the mitochondrial toxicity of the nucleoside drug, fialuridi
62         The cytotoxicity, neurotoxicity, and mitochondrial toxicity of up to 12 PFAS including perflu
63 cisplatin, HgCl(2), and gentamicin exhibited mitochondrial toxicity prior to decreases in basal respi
64 of triphosphate conversion, degradation, and mitochondrial toxicity remain.
65 erent activities of SSH1 in Abeta42O-induced mitochondrial toxicity remains unclear.
66               The primary outcome was severe mitochondrial toxicity (SMT) due to linezolid, defined a
67 fic target and active partner in mutant SOD1 mitochondrial toxicity suggests new therapeutic strategi
68 analogues that cause neuropathy exert direct mitochondrial toxicity that is not mediated indirectly t
69 ridine; FIAU) produce clinically significant mitochondrial toxicity that limits their dose or prevent
70 ism underlying intracellular Abeta42-induced mitochondrial toxicity through its impact on LONP1 and m
71 assay, subsequent screening of compounds for mitochondrial toxicity (uncoupling and inhibition), data
72 es to neurodegeneration through synaptic and mitochondrial toxicity via depletion of key proteins ess
73 utation R964C, which predisposes patients to mitochondrial toxicity when receiving 2',3'-didehydro-2'
74 nergic neuronal-specific dysfunction through mitochondrial toxicity, which can be attenuated by REST
75            Research has primarily focused on mitochondrial toxicity, which can cause death of the vul
76 scuous viral thymidine kinase and otherwise, mitochondrial toxicity would accumulate during long term
77 bitors, combined with propranolol, can cause mitochondrial toxicity, yielding potential clues about t