ライフサイエンスコーパス: hepatotoxicity

1 graine also suggests a reduced potential for hepatotoxicity.

2 inone-imines and, as such, the potential for hepatotoxicity.

3 ids dose-dependently induce PTB with minimal hepatotoxicity.

4 ted myeloid cells and macrophages and lethal hepatotoxicity.

5 g BA homoeostasis and protecting from the BA hepatotoxicity.

6 d the molecular mechanisms of TDCIPP-induced hepatotoxicity.

7 mice from lethal LPS/D-Galactosamine-induced hepatotoxicity.

8 ty, metastatic infection, nephrotoxicity, or hepatotoxicity.

9 abetes mellitus, cardiovascular disease, and hepatotoxicity.

10 147 when using nude mice with no evidence of hepatotoxicity.

11 ether the implicated agent is known to cause hepatotoxicity.

12 nificant risk factors for the development of hepatotoxicity.

13 iate inflammatory conditions in mice without hepatotoxicity.

14 h solubility, lack of CYP inhibition and low hepatotoxicity.

15 ly suitable for minimizing radiation-induced hepatotoxicity.

16 d CCL-4 were higher in subjects experiencing hepatotoxicity.

17 ency along with a higher propensity to cause hepatotoxicity.

18 hat manifests as severe photosensitivity and hepatotoxicity.

19 ling pathways without causing any detectable hepatotoxicity.

20 iabetes mellitus, cardiovascular disease, or hepatotoxicity.

21 levels and were predisposed to APAP-induced hepatotoxicity.

22 -mediated CYP450 induction, and drug-induced hepatotoxicity.

23 tor lepirudin and PAR-4 deficiency attenuate hepatotoxicity.

24 mice exhibited increased liver steatosis and hepatotoxicity.

25 osomal cholesterol (LC) accumulation in APAP hepatotoxicity.

26 n time and reduced immunogenicity as well as hepatotoxicity.

27 ven platelet activation participates in APAP hepatotoxicity.

28 rse reactions, including agranulocytosis and hepatotoxicity.

29 future therapeutic targets for APAP-induced hepatotoxicity.

30 lammation, liver neutrophil recruitment, and hepatotoxicity.

31 3 events of which one was a possibly related hepatotoxicity.

32 onhematopoietic cell PAR-4 signaling to APAP hepatotoxicity.

33 n patients without serious adverse events or hepatotoxicity.

34 fect of FABP1 on acetaminophen (AAP)-induced hepatotoxicity.

35 as sparse for some comparisons, particularly hepatotoxicity.

36 g, are a major mechanism contributing to BQA hepatotoxicity.

37 times the upper limit of normal or clinical hepatotoxicity.

38 euteration to reduce P450 metabolite-related hepatotoxicity.

39 effector differentiation resulting in overt hepatotoxicity.

40 ls to minimize off-target effects and reduce hepatotoxicity.

41 off-target toxicities, including concerns of hepatotoxicity.

42 d ROS and RNS for direct evaluation of acute hepatotoxicity.

43 ted with bacterial translocation during APAP hepatotoxicity.

44 possible that HMGB1 mediates gut BT in APAP hepatotoxicity.

45 ivated kinase (AMPK) in acetaminophen (APAP) hepatotoxicity.

46 x) 32, a key gap junction protein, to induce hepatotoxicity.

47 h increased liver triglyceride deposition or hepatotoxicity.

48 tioxidant and antitumour activities, without hepatotoxicity.

49 thout concomitant increase in the off-target hepatotoxicity.

50 mice were resistant to acetaminophen-induced hepatotoxicity.

51 licity contributes significantly to risk for hepatotoxicity.

52 nine nucleotide) consistent with AZA-induced hepatotoxicity.

53 ved transgene expression and largely avoided hepatotoxicity.

54 ptive response mechanisms in arsenic induced hepatotoxicity.

55 d-to-treat patients with severe APAP-induced hepatotoxicity.

56 d Fizz1, increased liver repair, and reduced hepatotoxicity.

57 trations that were paralleled by evidence of hepatotoxicity.

58 on, and protection of mice from APAP-induced hepatotoxicity.

59 a major role in acetaminophen (APAP)-induced hepatotoxicity.

60 NK activation and thus promotes drug-induced hepatotoxicity.

61 believed to be responsible for the observed hepatotoxicity.

62 nt hepatic failure and acetaminophen-induced hepatotoxicity.

63 brate, fully protects mice from APAP-induced hepatotoxicity.

64 er injury and in liver neutrophil influx and hepatotoxicity.

65 chloroquine further exacerbated APAP-induced hepatotoxicity.

66 utophagy by rapamycin inhibited APAP-induced hepatotoxicity.

67 the embolization materials exhibited evident hepatotoxicity.

68 ive diagnosis to some cases of presumed drug hepatotoxicity.

69 XCR2-FPR1 antagonism significantly prevented hepatotoxicity.

70 linically relevant sensitizer to TNF-induced hepatotoxicity.

71 r NAC-mediated recovery against APAP-induced hepatotoxicity.

72 l and microscopic data showed no evidence of hepatotoxicity.

73 ial adaptive response during alcohol-induced hepatotoxicity.

74 ccumulation that contributes to AhR-mediated hepatotoxicity.

75 EtOH-induced hepatic lipid accumulation and hepatotoxicity.

76 tribution and long half-life without obvious hepatotoxicity.

77 The only grade 3 or 4 adverse event was hepatotoxicity (10%).

78 ost common grade 3 and 4 adverse events were hepatotoxicity (188 [8%]), hypertension (99 [4%]), cardi

79 While 30 was found to have dose-limiting hepatotoxicity, 27 and its enantiomers exhibited limited

80 ALF etiologies included acetaminophen (APAP) hepatotoxicity (29%), indeterminate ALF (23%), idiosyncr

81 relationship between nucleotide sequence and hepatotoxicity, a structure-toxicity analysis was perfor

82 Hepatotoxicity accounts for a substantial number of drug

83 The absence of RelA resulted in hepatotoxicity across several models of pneumonia, sepsi

84 None of the preparations have shown hepatotoxicity against normal primary cells.

85 The primary safety endpoint was incidence of hepatotoxicity: alanine aminotransferase of greater than

86 Except in 1 child with hepatotoxicity, all adverse effects were mild and nonper

87 Secondary outcomes included incidence of hepatotoxicity (ALT > 1,000 IU/L), peak international no

88 Acetaminophen (APAP, paracetamol)-induced hepatotoxicity, although treatable by timely application

89 The side effects included 21 cases of hepatotoxicity and 3 cases of acute pancreatitis.

90 minophen (APAP) overdose is a major cause of hepatotoxicity and acute liver failure in the U.S., but

91 AP) overdose is one of the leading causes of hepatotoxicity and acute liver failure in the United Sta

92 event linking the bioactivation of drugs to hepatotoxicity and as a more direct and mechanistic indi

93 rted after liver failure due to drug-induced hepatotoxicity and certain viral infections.

94 chanisms associated with dronedarone-induced hepatotoxicity and clinical drug-drug interactions.

95 o evaluate the effects of CO on APAP-induced hepatotoxicity and CO's relationship to regulation of en

96 viral drug, is associated with idiosyncratic hepatotoxicity and dyslipidemia.

97 ular steatosis is a hallmark of drug-induced hepatotoxicity and early-stage fatty liver disease.

98 Drug-induced hepatotoxicity and fatty liver are the most relevant cau

99 ompounds exhibited in vitro neurotoxicity or hepatotoxicity and hence they had improved safety profil

100 ial in vivo safety of Gd-lip with respect to hepatotoxicity and immunopathology caused by inflammatio

101 ed protein-binding, substantially decreasing hepatotoxicity and improving the therapeutic index with

102 FK866 alleviated hepatotoxicity and increased autophagy while decreased J

103 To characterize hepatotoxicity and its outcomes from HDS versus medicati

104 racellular 4-HNE accumulation on TNF-induced hepatotoxicity and its potential implication in the path

105 We imaged drug-induced hepatotoxicity and its remediation longitudinally in mic

106 on in APAP-induced chemical stress, both the hepatotoxicity and localised Nrf2-luc response were amel

107 o the clinical presentation of acetaminophen-hepatotoxicity and may inform future mechanistic studies

108 el mechanism underlying alpha-GalCer-induced hepatotoxicity and MDSC accumulation.

109 xicity in rats included loss of body weight, hepatotoxicity and nephrotoxicity.

110 tment, after administration of the codrug no hepatotoxicity and no induction of the cytochrome P450 s

111 ously evaluate the drug anti-tumor activity, hepatotoxicity and pharmacokinetics.

112 ded at least 1 of 2 prespecified end points (hepatotoxicity and prevention of active TB).

113 s from the areas of preclinical and clinical hepatotoxicity and safety assessment, from industry, aca

114 oxygen species generated during drug-induced hepatotoxicity and suggest that induction of UCP2 may al

115 om a polyfunctional T cell activation caused hepatotoxicity and the rapid induction of apoptotic sign

116 dentify novel genes involved in APAP-induced hepatotoxicity and to provide potential targets to devel

117 dospicine is consistent with observed canine hepatotoxicity, and considering the higher in vitro tran

118 um T3 (3,3 ,5-triiodo-l-thyronine), maternal hepatotoxicity, and increased multinucleated germ cells

119 , reliability, active TB disease, mortality, hepatotoxicity, and other harms.

120 are unreactive with thiols, display reduced hepatotoxicity, and retain Hsp90 and growth-inhibitory a

121 monocyte-derived macrophages aggravate APAP hepatotoxicity, and the pharmacological inhibition of ei

122 for MLK3 in APAP-induced JNK activation and hepatotoxicity, and they suggest MLK3 as a possible targ

123 LNA modified ASOs can cause hepatotoxicity, and this risk is currently not fully und

124 RF1 delivery to Junb-deficient mice restored hepatotoxicity, and we demonstrate that Ifng is a direct

125 epatitis C virus (HCV) disease, drug-induced hepatotoxicity, and, possibly, direct damage from HIV in

126 ts that seem to have the least potential for hepatotoxicity are citalopram, escitalopram, paroxetine,

127 Reliable test systems to identify hepatotoxicity are essential to predict unexpected drug-

128 depressants associated with greater risks of hepatotoxicity are iproniazid, nefazodone, phenelzine, i

129 sing rAAV-shRNAs we have now determined that hepatotoxicity arises when exogenous shRNAs exceed 12% o

130 e in JQ1 delivery to the liver, there was no hepatotoxicity as evidenced by H&E staining and little i

131 in productions were monitored during a 5-day hepatotoxicity assessment in which human primary hepatoc

132 ch can induce anti-tuberculosis drug-induced hepatotoxicity (ATDH) and SCZ-like disorders.

133 A inhibition is useful for alleviating acute hepatotoxicity attributed to APAP overdose.

134 gion have been associated with idiosyncratic hepatotoxicity attributed to flucloxacillin, ximelagatra

135 s from HDS versus medications, patients with hepatotoxicity attributed to medications or HDS were enr

136 hed hepatic NADP and protected the mice from hepatotoxicity, based on markers such as increased level

137 hepatotoxicity of TDCIPP, the expression of hepatotoxicity biomarker genes, liver histopathology and

138 It has been implicated to have hepatotoxicity, but its molecular mechanisms remain uncl

139 ined JNK activation plays a critical role in hepatotoxicity by acetaminophen or GalN/TNF-alpha.

140 cumulation determines susceptibility to APAP hepatotoxicity by modulating mitophagy, and imply that g

141 Protection against hepatotoxicity by UCP2-induction through activation of P

142 es for antiretroviral therapy, but can cause hepatotoxicity by unknown mechanisms.

143 ing high affinity modifications such as LNA, hepatotoxicity can occur as a result of unintended off-t

144 Induced Liver Injury Network (DILIN) studies hepatotoxicity caused by conventional medications as wel

145 Hepatotoxicity caused by HDS was evaluated by expert opi

146 Mechanism profiling of hepatotoxicity caused by oxidative stress using antioxid

147 Emergence of mixed or cholestatic hepatotoxicity caused the data monitoring committee to s

148 ury," "liver failure," "DILI," "hepatitis," "hepatotoxicity," "cholestasis," and "aminotransferase,"

149 he diurnal variation in acetaminophen (APAP) hepatotoxicity (chronotoxicity) reportedly is driven by

150 ficantly with less bone destruction and less hepatotoxicity compared with equimolar doses of free doc

151 The extract did not present hepatotoxicity, confirming the possibility of its applic

152 ironmental and pharmaceutical compounds with hepatotoxicity data.

153 ice, however, were sensitive to APAP-induced hepatotoxicity despite activation of PPARalpha with Wy-1

154 nthesized for duplex imaging of drug-induced hepatotoxicity (DIH), a long-term medical concern.

155 nti-pain/fever drug paracetamol often causes hepatotoxicity due to peroxynitrite ONOO(-) .

156 clinical management of patients experiencing hepatotoxicity during lapatinib treatment.

157 SMase(-/-) mice and hepatocytes against APAP hepatotoxicity, effects that were reversed by chloroquin

158 umab ozogamicin is associated with increased hepatotoxicity, especially after follow-up HSCT, compare

159 All antidepressants can induce hepatotoxicity, especially in elderly patients and those

160 ns of an extensive antioxidant screening and hepatotoxicity evaluation against HepG2, a human hepatob

161 g set of in vivo rodent experiments for drug hepatotoxicity evaluation, we discovered common biomarke

162 del at low dosage (0.1 mg/kg, i.p.), lacking hepatotoxicity even at high dose (3 mg/kg, i.p.).

163 e viral hepatitis coinfections, drug-related hepatotoxicity, fatty liver disease, and direct and indi

164 y every patient deemed to be at any risk for hepatotoxicity following acetaminophen overdose.

165 xidative metabolism are be more sensitive to hepatotoxicity following PERC exposure.

166 Concerns related to hepatotoxicity frequently lead to discontinuation or non

167 n during NAC treatment can discriminate APAP hepatotoxicity from ischemic hepatitis.

168 to an examination of autophagy's function in hepatotoxicity from proinflammatory cytokines.

169 he expression of several biomarker genes for hepatotoxicity (gck, gsr and nqo1) and caused hepatic va

170 67 mug/mL, respectively) cell lines, without hepatotoxicity (GI(50)>400 mug/mL).

171 iral load (>4.39 log copies/mL), more severe hepatotoxicity grade, and increased likelihood of ALT >=

172 Neither arm had any hepatotoxicity, grade 4 AEs, or treatment-attributed dea

173 ssays/techniques in order to investigate the hepatotoxicity; however, only the covalent binding in ra

174 nd management of ICI-induced immune-mediated hepatotoxicity (IMH), including approaches to treatment

175 secondary plant metabolites which can cause hepatotoxicity in both humans and livestock.

176 xperimental pulmonary hypertension but cause hepatotoxicity in clinical studies.

177 No patients developed hepatic injury or hepatotoxicity in either group (odds ratio 1.0 [95% conf

178 ther APAP can modulate autophagy to regulate hepatotoxicity in hepatocytes.

179 Thus, this model allows for investigation of hepatotoxicity in human liver tissue upon applying drug

180 ion are likely to be critical events in APAP hepatotoxicity in humans, resulting in necrotic cell dea

181 ondria are central in the mechanisms of APAP hepatotoxicity in humans.

182 nd validate the mechanism of tacrine-induced hepatotoxicity in Lister hooded rats.

183 e nanoprobes achieve real-time monitoring of hepatotoxicity in living animals, thereby providing a co

184 othiols, for early detection of drug-induced hepatotoxicity in living mice.

185 Numerous studies have shown that APAP hepatotoxicity in mice involves mitochondrial dysfunctio

186 on of key temporal features of acetaminophen hepatotoxicity in mice.

187 sified based upon the presence or absence of hepatotoxicity in mice.

188 evation and caspase activation in cells, and hepatotoxicity in mice.

189 requency of, and potential risk factors for, hepatotoxicity in patients in this trial and after treat

190 e effective noninvasive tools for monitoring hepatotoxicity in patients receiving methotrexate for ps

191 e is a need for noninvasive tools to monitor hepatotoxicity in patients with psoriasis who are receiv

192 modified ASOs and decrease the likelihood of hepatotoxicity in preclinical testing.

193 tudies have shown FG or Geniposide can cause hepatotoxicity in rats.

194 protected wildtype mice against APAP-induced hepatotoxicity in the absence of PPARalpha activation.

195 Hepatotoxicity in the absence of RelA could be reversed

196 iver injury now accounts for 20% of cases of hepatotoxicity in the United States based on research da

197 tal admission and the most frequent cause of hepatotoxicity in the Western world.

198 on, neuroprotective effects, lacks tacrine's hepatotoxicity in vitro and in vivo, and shows the same

199 olysaccharide/D-galactosamine (GalN)-induced hepatotoxicity in vitro and in vivo.

200 ort a luminescent approach to evaluate acute hepatotoxicity in vivo by chromophore-conjugated upconve

201 o, and attenuates PXR-mediated acetaminophen hepatotoxicity in vivo.

202 real-time unambiguous visualization of such hepatotoxicity in vivo.

203 racterizes a novel mechanism of drug-induced hepatotoxicity in which mithramycin not only alters farn

204 PP induces hepatic inflammation and leads to hepatotoxicity in zebrafish.

205 first treatment, 13 (1%) of 996 patients had hepatotoxicity (including one [<1%] possible Hy's law ca

206 bes investigator-assessed treatment-emergent hepatotoxicity, including sinusoidal obstruction syndrom

207 ammatory macrophages have been implicated in hepatotoxicity induced by the analgesic acetaminophen (A

208 APAP hepatotoxicity-induced liver regeneration involves a com

209 toposide group (cardiac arrest, dehydration, hepatotoxicity, interstitial lung disease, pancytopenia,

210 RIP3 is an early mediator of APAP hepatotoxicity, involving modulation of mitochondrial dy

211 nd functional outcomes; mixed or cholestatic hepatotoxicity is an identified risk.

212 Hepatotoxicity is an important irAE, occurring in up to

213 Acetaminophen (APAP) hepatotoxicity is associated with a high rate of gram-ne

214 hramycin-induced transaminitis revealed that hepatotoxicity is associated with germline variants in g

215 strate that the off-target RNA knockdown and hepatotoxicity is attenuated by RNase H1 knockdown, and

216 f compensatory liver regeneration after APAP hepatotoxicity is critical for final recovery, but the m

217 Using traditional animal models to detect hepatotoxicity is expensive and time-consuming.

218 Standard preclinical evaluation of drug hepatotoxicity is generally performed using in vivo anim

219 he role of lysosomes in acetaminophen (APAP) hepatotoxicity is poorly understood.

220 stage IV and III melanoma.(1) Immune-related hepatotoxicity is reported in 2-10% of patients(2) with

221 Liver toxicity (hepatotoxicity) is a critical issue in drug discovery an

222 reported to be responsible for APAP-induced hepatotoxicity, it is not known whether APAP can modulat

223 g/day are associated with increased risk for hepatotoxicity, many drugs are safe at such dosages.

224 o exhibited significantly elevated levels of hepatotoxicity markers in circulation, a 58% increase in

225 In a cellular hepatotoxicity model, analyzing the influence on viabili

226 nistration, which is usually associated with hepatotoxicity, nephrotoxicity and hemolysis.

227 in patients with and without SRI, including hepatotoxicity, nephrotoxicity, any reported AE, mortali

228 nized mouse models, we recapitulated the RTV hepatotoxicity observed in the clinic.

229 Multiple clinical studies found that hepatotoxicity occurred in 100% of participants who were

230 oral medications and observed high risk for hepatotoxicity (odds ratio [OR], 14.05; P < 0.001) for d

231 The direct hepatotoxicity of APAP triggers a cascade of innate immu

232 moderate ethanol did not increase the direct hepatotoxicity of CCl4.

233 s represents a powerful tool to evaluate the hepatotoxicity of drugs that are metabolized by CYP2E1.

234 tasis is reported along with a review of the hepatotoxicity of other PKIs.

235 convenient screening strategy for assessing hepatotoxicity of synthetic drugs.

236 nt gut microbial influences in modifying the hepatotoxicity of tacrine, providing insights for person

237 iver-gut microbiota axis in underpinning the hepatotoxicity of tacrine.

238 To further characterize the hepatotoxicity of TDCIPP, the expression of hepatotoxici

239 for clinician awareness regarding potential hepatotoxicity of varenicline, particularly among patien

240 Treatment-emergent hepatotoxicities (of all grades) were more frequent in t

241 of normal indicative of mixed or cholestatic hepatotoxicity, one lasting 7 months and confirmed by bi

242 (-/-) animals are resistant to acetaminophen hepatotoxicity or fasting-induced steatosis.

243 ect outcomes in the context of acetaminophen hepatotoxicity or hepatic ischemia-reperfusion injury.

244 rule-of-two positives being associated with hepatotoxicity (OR, 3.89; P < 0.01).

245 osis in tumors without inducing weight loss, hepatotoxicity, or inflammation.

246 ith adverse drug reactions (ADRs), including hepatotoxicity; oxidative metabolism of 1 has been impli

247 plasma of wild-type mice with acetaminophen hepatotoxicity (P<0.05).

248 andardized system for categorizing drugs for hepatotoxicity potential will help develop objective and

249 ritical protective role against APAP-induced hepatotoxicity, primary cultured mouse hepatocytes and g

250 To overcome the recent outbreaks of hepatotoxicity-related drugs, a new analytical tool for

251 Again, the rule-of-two predicted hepatotoxicity reliably.

252 Current drug-safety assays for hepatotoxicity rely on biomarkers with low predictive po

253 Isoniazid (INH)-induced hepatotoxicity remains one of the most common causes of

254 ch as Parkinson's disease, due to the severe hepatotoxicity risk associated with tolcapone.

255 lly explore the application of stem cells in hepatotoxicity safety assessment and to make recommendat

256 complementary to animal testing, for initial hepatotoxicity screening or mechanistic studies of candi

257 Organotypic liver culture models for hepatotoxicity studies that mimic in vivo hepatic functi

258 ite alterations associated with hallmarks of hepatotoxicity such as gamma-glutamyl dipeptides, acylca

259 Recently, a liver tissue model conducive to hepatotoxicity testing was developed by bioprinting hepa

260 Isoniazid is associated with higher rates of hepatotoxicity than placebo or rifampin.

261 ong cholinesterase inhibitory activity, less hepatotoxicity than tacrine, and the best neuroprotectiv

262 peutic dose is limited by the development of hepatotoxicity that remains poorly characterized.

263 In acetaminophen-hepatotoxicity, the mechanism by which tissue cohesion a

264 , or R341C in mice predisposes to acute APAP hepatotoxicity, thereby providing direct evidence for th

265 cine group vs nine in the placebo group) and hepatotoxicity (three vs one).

266 tent environmental contaminant which elicits hepatotoxicity through activation of the aryl hydrocarbo

267 PXR was found to modulate RTV hepatotoxicity through CYP3A4-dependent pathways involve

268 hese results suggest that mithramycin causes hepatotoxicity through derangement of bile acid disposit

269 ombination of high potency to tumors and low hepatotoxicity to provide a pronounced survival benefit

270 In order to understand the mechanism of this hepatotoxicity, transcriptional profiles were collected

271 inhibitors used were shown to cause relevant hepatotoxicity under nearly all conditions, but particul

272 se 3 (GSK3) in liver regeneration after APAP hepatotoxicity using a pharmacological inhibition strate

273 d the effect of bile acid modulation on APAP hepatotoxicity using C57BL/6 mice, which were fed a norm

274 ve potential of IL-22 in murine APAP-induced hepatotoxicity was assessed.

275 The highest risk of hepatotoxicity was associated with azathioprine and infl

276 ical and hepatocellular carcinomas), and the hepatotoxicity was evaluated using a porcine liver prima

277 ical and hepatocellular carcinomas), and the hepatotoxicity was evaluated using a porcine liver prima

278 er a median follow-up period of 14.7 months, hepatotoxicity was found to be a frequent and often seve

279 Multiple lines of evidence suggest that this hepatotoxicity was immune mediated.

280 TG can be used safely and the occurrence of hepatotoxicity was low.

281 to tumor lysis syndrome, overall nephro- and hepatotoxicity was low.

282 he chronic toxicity of fialuridine for which hepatotoxicity was mimicked after repeated-dosing in the

283 Hepatotoxicity was observed in humans at daily doses of

284 Hepatotoxicity was observed in oral and inhalation expos

285 Whilst ajmaline-related hepatotoxicity was well-recognised in the era in which t

286 f phenolics (SP2) against CCl4-induced acute hepatotoxicity were evaluated in rats.

287 s), the most relevant bioassay(s) related to hepatotoxicity were identified.

288 me and the role of CYP2E1 in ethanol-induced hepatotoxicity were investigated using liquid chromatogr

289 isturbances, syncope, myasthenia gravis, and hepatotoxicity were noted.

290 ein adduct-specific serum immunoglobulin and hepatotoxicity were reduced.

291 Safety measures, including hepatotoxicity, were not different.

292 r lipophilicity, with negligible nephro- and hepatotoxicities when administered intravenously.

293 Paracetamol (APAP) has been known to induce hepatotoxicity when exceeding therapeutic doses and was

294 ered 90 minutes post-APAP) protected against hepatotoxicity, whereas mice treated with APAP alone dev

295 sential roles of human PXR and CYP3A4 in RTV hepatotoxicity, which can be applied to guide the safe u

296 not secondary to alteration of APAP-induced hepatotoxicity, which remained unchanged after GSK3 inhi

297 er mitochondrial activity and reduced CCl(4) hepatotoxicity with improved blood levels of aspartate a

298 on, resulting in defective BA metabolism and hepatotoxicity with inflammation.

299 n focused on investigating the mechanisms of hepatotoxicity, with limited success in advancing therap

300 aracteristic spatiotemporal features of APAP hepatotoxicity within hepatic lobules.