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1 onavir and remdesivir, which are potentially hepatotoxic.
2 be one of the mechanisms by which ethanol is hepatotoxic.
3 old lower vector dose was significantly less hepatotoxic.
4 rather than STAT3 to signal, was found to be hepatotoxic.
5                      However, statins can be hepatotoxic.
6 e FMOs metabolites seem to be neurotoxic and hepatotoxic.
7 nd the alternative--propylthiouracil--can be hepatotoxic.
8  a commonly used analgesic, it can be highly hepatotoxic.
9 mulation in the liver, and excessive iron is hepatotoxic.
10 ins free nicotinic acid, but some brands are hepatotoxic.
11 stinal, two allergic); three late syndromes (hepatotoxic, accelerated nephrotoxic, erythromelalgia);
12   Treatment of hepatocyte-derived cells with hepatotoxic acetaminophen (APAP) induces a biphasic prot
13 inds and inactivates the highly reactive and hepatotoxic acetaminophen metabolite N-acetyl-p-benzoqui
14 odels with a transient regimen of moderately hepatotoxic acetaminophen.
15                                              Hepatotoxic aflatoxins have found a worthy adversary in
16 ly promotes liver damage and is not a direct hepatotoxic agent.
17 mal manifestations require the withdrawal of hepatotoxic agents and the reversal of hepatic iron over
18             Chronic exposure of the liver to hepatotoxic agents initiates an aberrant wound healing r
19                            A number of other hepatotoxic agents, such as d-galactosamine, CCl4, and t
20 fects of acetaminophen and potentially other hepatotoxic agents.
21 here it is known to potentiate the action of hepatotoxic agents.
22 l-para-aminophenol (APAP, or paracetamol), a hepatotoxic analgesic drug.
23 y bile acid lithocholic acid (LCA), which is hepatotoxic and a potential enteric carcinogen.
24                     Aflatoxin B1 (AFB1) is a hepatotoxic and carcinogenic food contaminant.
25                                  The lack of hepatotoxic and general toxic effects makes A250 an exce
26 Beyond normal therapeutic doses, the drug is hepatotoxic and genotoxic.
27  agonist of the nuclear receptor FXR was not hepatotoxic and had no regulatory effects.
28  mouse liver following administration of non-hepatotoxic and hepatotoxic doses in vivo, implying that
29                 Unfortunately, dantrolene is hepatotoxic and unsuitable for chronic long-term adminis
30  derivative lithocholic acid (LCA) is highly hepatotoxic and, as we show here, a metabolic substrate
31                                      MCs are hepatotoxic, and acute exposure causes severe liver dama
32  shown harmful effects, such as nephrotoxic, hepatotoxic, and genotoxic effects, in humans due to the
33 ial for apoptosis-inducing activity of a non-hepatotoxic anti-Fas mAb HFE7A.
34 ompared to Vancomycin, which was found to be hepatotoxic at similar concentrations.
35 ged liver microenvironment was not, however, hepatotoxic, because CBLB502 induced resistance to Fas-m
36 -dose UDCA could result in the production of hepatotoxic bile acids, such as lithocholic acid (LCA),
37 holestasis to diminish uptake of potentially hepatotoxic bile acids.
38 tics of HDS users and users of 6 potentially hepatotoxic botanical products were compared with non-HD
39 eous healing in experimental mouse models of hepatotoxic (carbon tetrachloride [CCl(4)] intoxication)
40 result from the joint effects of viruses and hepatotoxic chemical carcinogens.
41  nonimmunologically by chronic exposure to a hepatotoxic chemical.
42                                     Grouping hepatotoxic chemicals based on the chemical structure re
43 ary epithelial cells are targets for certain hepatotoxic chemicals, including some procarcinogens, th
44  as MeOH-2, and MeOH-3, completely devoid of hepatotoxic components.
45 re we show that treatment with two different hepatotoxic compounds (acetaminophen and thioacetamide)
46 l genomic prediction technique for screening hepatotoxic compounds based on in vitro human liver cell
47 ning technique that can identify potentially hepatotoxic compounds in the early stages of drug develo
48 trum, the relative contents of the potential hepatotoxic compounds pulegone and menthofuran were redu
49 is B virus infection and dietary exposure to hepatotoxic contaminants.
50                       Microcystins (MCs) are hepatotoxic cyclic heptapeptides produced by cyanobacter
51 ystems and influences liver repair following hepatotoxic damage or regeneration following partial hep
52                          Administration of a hepatotoxic diet containing 0.1% 3,5-diethoxycarbonyl-1,
53 oagulation (FXI) pathway were administered a hepatotoxic dose of 400 mg/kg of APAP.
54 .4 mg/mL, 8 microL/h) 4 to 16 hours before a hepatotoxic dose of acetaminophen (600 mg/kg, intraperit
55 lowing administration of non-hepatotoxic and hepatotoxic doses in vivo, implying that Nrf2 may have a
56                                              Hepatotoxic doses of acetaminophen to mice produce not o
57 in rats and several patients after consuming hepatotoxic doses of APAP.
58  liver injury, rats were treated either with hepatotoxic doses of D-(+)-galactosamine (DGAL) or aceta
59  TNF-alpha before administration of low, but hepatotoxic, doses of CCl4.
60 ed hepatocellular disease by administering a hepatotoxic drug and compared the hepatic extraction eff
61 ate production caused by the addition of the hepatotoxic drug Bosentan was determined.
62               Dogs that were affected by the hepatotoxic drug had reduced HEE.
63 s progression of liver injury even after the hepatotoxic drug is cleared from the body.
64                  Cocaine is a widely abused, hepatotoxic drug without an FDA-approved pharmacotherapy
65 ), or 2-propylpentanoic acid, a prototypical hepatotoxic drug.
66  toxicity analysis was performed for fifteen hepatotoxic drugs by evaluating toxic changes reflecting
67 applied to clinical case studies to identify hepatotoxic drugs in complex comedication regimes to fur
68                           Failure to predict hepatotoxic drugs in preclinical testing makes it impera
69         The risk associated with exposure to hepatotoxic drugs is difficult to quantify.
70               Acute liver failure induced by hepatotoxic drugs results from rapid progression of inju
71  the development of ACLF in this population, hepatotoxic drugs should be avoided, it is recommended t
72  = 81), subjects who safely took potentially hepatotoxic drugs without adverse effects (n = 55 and n
73 ule-of-two positives, 14 were withdrawn from hepatotoxic drugs, and one was over-the-counter medicati
74 ed number of patients prescribed potentially hepatotoxic drugs, including simvastatin (14 036 024 [95
75 ld-type mice when co-administered with known hepatotoxic drugs.
76 T observed in some patients suggested a mild hepatotoxic effect of IFN.
77  cycloheximide, thus suggesting the indirect hepatotoxic effect of MIP2.
78  while chronic exposure produces only a rare hepatotoxic effect.
79 g polygenic risk scores were associated with hepatotoxic effects across all therapy phases and were l
80 P, which c) elicited maternal thyrotoxic and hepatotoxic effects and d) induced MNGs in the fetal tes
81 tent pollutants that have been shown to have hepatotoxic effects in animal models.
82      Perfluorooctanoic acid (PFOA or C8) has hepatotoxic effects in animals.
83 , transcriptomic analysis revealed potential hepatotoxic effects in exposed larvae, including macrove
84                The long-term implications of hepatotoxic effects in patients with psoriasis remains u
85                                              Hepatotoxic effects of APAP-mediated Ca2+ deregulation w
86 of c-Jun N-terminal kinase (JNK) mediate the hepatotoxic effects of APAP.
87 re, postulated that DC may also modulate the hepatotoxic effects of APAP.
88 nce of the livers may have resulted from the hepatotoxic effects of chemotherapy and/or hepatic infil
89 creased risk who are most susceptible to the hepatotoxic effects of excess alcohol consumption or obe
90         Lipidomic analysis revealed that the hepatotoxic effects of prometryn are associated with inc
91  Liver injury is thought to be caused by the hepatotoxic effects of the retained alpha1-ATZ.
92 npredictable nature of many of the potential hepatotoxic effects of these agents, especially in cases
93  GstP null mice were highly resistant to the hepatotoxic effects of this compound.
94 und to be considerably less sensitive to its hepatotoxic effects than wild-type animals, indicating t
95 suppression, sepsis, pneumotoxic effects, or hepatotoxic effects within 90 days of starting the study
96 , monitor for the development of MTX-induced hepatotoxic effects, and monitor for worsening of hepati
97                                              Hepatotoxic effects, including hyperbilirubinemia and el
98                    Little is known about its hepatotoxic effects, which we aimed to characterize in t
99 abortifacient despite its potentially lethal hepatotoxic effects.
100                            Grade 3 or higher hepatotoxic events occurred in 11.7% of participants ove
101 ulation of LP-Z in the circulation, which is hepatotoxic from excessive FC.
102 es reduced or eliminated toxicity of several hepatotoxic gapmer ASOs.
103 ot provide any indication that FIAU would be hepatotoxic in humans.
104  first time in detail, may contribute to the hepatotoxic, inflammatory, and tumorigenic action of MC-
105 stress, reactive oxygen species, and causing hepatotoxic injury by alcohol and various hepatotoxins.
106 Oral administration of VLX103 also decreased hepatotoxic injury in a second more chronic model of alc
107 ess tissue damage and improved survival in a hepatotoxic injury model.
108  that liver regeneration induced by an acute hepatotoxic injury promotes expansion of transplanted he
109                                              Hepatotoxic insults often lead to an impairment of mitoc
110                     According to this model, hepatotoxic insults select for hepatocytes with specific
111 has been reported to protect against various hepatotoxic insults, influences the susceptibility of mi
112 , we have identified a novel and potentially hepatotoxic interaction that might occur during concomit
113 estingly, Gadd45beta ablation did not affect hepatotoxic JNK signaling after a TNFR-mediated immune c
114 this drug in the prevention and treatment of hepatotoxic liver injury.
115                      Thus, rather than being hepatotoxic, liver triglyceride accumulation is actually
116 ranscript knockdown in mice treated with non-hepatotoxic LNA ASOs, while the levels of many unintende
117 nel of highly efficacious hepatotoxic or non-hepatotoxic LNA ASOs.
118 ranscripts were reduced in mice treated with hepatotoxic LNA ASOs.
119                                  We examined hepatotoxic mechanisms in mice homozygous for the severe
120 demographic data, including body mass index, hepatotoxic medication use, and alcohol intake, were ana
121 as issues surrounding the use of potentially hepatotoxic medications in patients with underlying chro
122            With respect to using potentially hepatotoxic medications in patients with underlying live
123              Finally, the use of potentially hepatotoxic medications in patients with underlying live
124                       The use of potentially hepatotoxic medications in patients with underlying live
125  included: history of hepatitis, exposure to hepatotoxic medications, prior weight loss surgery, and
126 cause of insufficient liver tissue or use of hepatotoxic medications, so 148 remained in the study (m
127                                  Patients on hepatotoxic medications, such as HIV and TB medications,
128 cule that, unlike ApAP, does not produce the hepatotoxic metabolite N-acetyl-p-benzoquinone-imine (NA
129 required for the transformation of APAP to a hepatotoxic metabolite, Cypor-deficient cells are protec
130 tabolic conversion of the drug to its active hepatotoxic metabolite.
131 -, and CYP3A4-driven conversion of APAP into hepatotoxic metabolites.
132 For example, members of a few genera produce hepatotoxic microcystins, whereas production of hepatoto
133                        Using cholestatic and hepatotoxic models of liver injury, we compared the deve
134                                   In various hepatotoxic models, both pro- and anti-inflammatory acti
135 asing the expression and accumulation of the hepatotoxic mutant protein.
136 atotoxic microcystins, whereas production of hepatotoxic nodularins appears to be limited to a single
137 e treated with a panel of highly efficacious hepatotoxic or non-hepatotoxic LNA ASOs.
138  but also differences in the intake of other hepatotoxic or protective factors, differences in the ce
139 Predictor provides mechanistic insights into hepatotoxic pathways, enabling early de-risking and acti
140 research into how these reactions respond to hepatotoxic pharmaceuticals.
141 -treated Era(-/-) mice developed none of the hepatotoxic phenotypes such as hepatomegaly, elevation i
142 or Z a1-antitrypsin (ATZ), a protein forming hepatotoxic polymers retained in the endoplasmic reticul
143                                          The hepatotoxic potential of 3-hydroxy-3-methylglutaryl coen
144       Recent studies have raised concerns of hepatotoxic potential related to the use of fluoroquinol
145 tive ability of HCV-specific T cells and the hepatotoxic potential that they possess, there is a grea
146    CBD, CBN, and CBG demonstrated the lowest hepatotoxic potential, as evidenced by unchanged liver i
147 s a more direct and mechanistic indicator of hepatotoxic potential.
148 okine milieu drive both hepatoprotective and hepatotoxic processes.
149 olic profile, antioxidant, antibacterial and hepatotoxic properties were analyzed.
150 and 0.15% of those completing treatment) had hepatotoxic reactions to isoniazid during preventive tre
151 kaloids (PAs) and their N-oxides (PANOs) are hepatotoxic secondary metabolites present in certain pla
152 and investigated the potential mechanisms of hepatotoxic sensitivity.
153 tifs (TCC and TGC) that were present only in hepatotoxic sequences.
154              Tolcapone is also known for its hepatotoxic side effects even though it is therapeutical
155 t graft-protective attributes and the lowest hepatotoxic side effects.
156 e was demonstrated to be a safe drug without hepatotoxic side effects.
157   We developed SRP-001, a non-opioid and non-hepatotoxic small molecule that, unlike ApAP, does not p
158 ny older agents, in some cases expanding the hepatotoxic spectrum for the drugs.
159                           In mice, different hepatotoxic stimuli linked with the development of diffe
160 dose >50 mg (n = 50) were significantly more hepatotoxic than compounds belonging to other groups.
161 drate-derived palmitate in the liver is more hepatotoxic than dietary palmitate.
162           However, only one of them was less hepatotoxic than tacrine in HepG2 cells.
163 lipids and their metabolites are potentially hepatotoxic, the absence of overt injury in fatty livers
164 patitis viruses appear to be synergistically hepatotoxic; this synergy appears to explain both the hi
165             These data strongly suggest that hepatotoxic TRO causes apoptosis by activating the JNK-d
166 ydroxylation, leading to the accumulation of hepatotoxic unsaturated monohydroxy bile acids.
167  common fever medicine acetaminophen becomes hepatotoxic via cytochrome p450 metabolism.
168  elicits metabolic perturbations that may be hepatotoxic, we investigated the relationship between fr

 
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