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1 nd reduced liver damage in mice exposed to a hepatotoxin.
2 ethionine has been identified as a potential hepatotoxin.
3 how that species-matched IL11 behaves like a hepatotoxin.
4  and cholestasis, when exposed to nine known hepatotoxins.
5 though some had exposures to other potential hepatotoxins.
6 iver-specific products and susceptibility to hepatotoxins.
7 ng hepatotoxic injury by alcohol and various hepatotoxins.
8 ought to light a few new agents as potential hepatotoxins.
9 event in liver necrosis caused by alkylating hepatotoxins.
10 athology in response to ischemia and certain hepatotoxins.
11 vels found in the liver after treatment with hepatotoxins.
12 to steatosis and increased susceptibility to hepatotoxins.
13 ittermates were challenged by feeding with a hepatotoxin 3,5-diethoxycarbonyl-1,4-dihydrocollidine (D
14                     Liver injury, induced by hepatotoxin 3,5-diethoxycarbonyl-1,4-dihydrocollidine (D
15  human FL-HCC, as well as treatment with the hepatotoxin 3,5-diethoxycarbonyl-1,4-dihydrocollidine, w
16 g administration of the metabolism-dependent hepatotoxin acetaminophen (APAP) or the direct nephrotox
17 lso enhance sensitivity to the albumin-bound hepatotoxin, acetaminophen (APAP).
18 t Fxralpha-/- mice, after treatment with the hepatotoxin alpha-naphthylisothiocyanate, which is known
19 gal blooms, exposure to microcystin, a known hepatotoxin and a byproduct of cyanobacterial blooms can
20               Aflatoxin B1 (AFB1) is a human hepatotoxin and hepatocarcinogen produced by the mold As
21  data suggest that species-matched IL11 is a hepatotoxin and that IL11 signaling might be an effectiv
22 for patients with NAFLD include avoidance of hepatotoxins and aggressive management of associated con
23 tochrome P450 2E1 (CYP2E1) activates several hepatotoxins and contributes to alcoholic liver damage.
24 be important in CYP2E1-catalyzed toxicity of hepatotoxins and in alcohol-induced liver injury.
25                                        Since hepatotoxins are associated with increased keratin phosp
26 ynthesis of cylindrospermopsin (1), a potent hepatotoxin associated with the cyanobacterium Cylindros
27                   Another 7 (2%) were direct hepatotoxins but only in high doses and placed in a sepa
28                       Alcohol functions as a hepatotoxin by overwhelming cell stress response pathway
29 ound in water bodies and their production of hepatotoxins can contribute to liver damage.
30 ntrols before and after a single dose of the hepatotoxin carbon tetrachloride and hybridized them aga
31 12 weeks by intraperitoneal injection of the hepatotoxin carbon tetrachloride.
32  after chronic injury inflicted by iterative hepatotoxin (carbon tetrachloride) injection and bile du
33 l animals following exposure to the chemical hepatotoxin, carbon tetrachloride (CCl4).
34                                          The hepatotoxin CCl(4) induced activation of RSK, phosphoryl
35 pressed inflammatory responses in a model of hepatotoxin (CCl4 )-induced hepatitis, but surprisingly
36 rious conditions, including systemic injury, hepatotoxin exposure, and warm ischemia.
37 charide (LPS) alone or LPS together with the hepatotoxin galactosamine (GalN) was performed to identi
38 ver, exposure of S52A-expressing mice to the hepatotoxins, griseofulvin or microcystin, which are ass
39           This microcystin analog and potent hepatotoxin has previously been known only from the aqua
40 of urine following administration of a model hepatotoxin hydrazine.
41 strate that the production of cyanobacterial hepatotoxins in lichen symbiosis is a global phenomenon
42  to COL1 were more resistant to a variety of hepatotoxins, in a dose-dependent manner, and had lower
43 several new reports of previously recognized hepatotoxins, including herbal products, were published.
44 aling provides hepatocyte protection against hepatotoxin-induced apoptosis.
45 ollowing intravenous injection) detection of hepatotoxin-induced liver fibrosis using T(1)-weighted M
46 ytokine but is hepatoprotective in models of hepatotoxin-induced liver fibrosis.
47 revents T/NKT cell hepatitis but exacerbates hepatotoxin-induced liver injury by inhibiting macrophag
48 lished prednisolone-mediated exacerbation of hepatotoxin-induced liver injury.
49 oxl1-expressing cells are not the origin for hepatotoxin-induced liver tumors.
50  that i.v. delivery of asparagine can dampen hepatotoxin-induced pericentral hepatocellular death.
51 neages during liver injury in the context of hepatotoxin-inhibited hepatocyte proliferation.
52  data identify FKB as a potent GSH-sensitive hepatotoxin, levels of which should be specifically moni
53 found that, after fibrotic liver injury from hepatotoxins, LSECs become highly proinflammatory and se
54 tecting all the 11 tested commonly occurring hepatotoxins (MC-LR, -dmlR, -RR, -dmRR, -LA, -LY, -LF, -
55 alpha-galactosylceramide (alpha-GalCer), and hepatotoxin-mediated hepatitis induced by carbon tetrach
56 4)) were employed to induce cholestatic- and hepatotoxin-mediated liver fibrosis, respectively.
57 e display library against the cyanobacterial hepatotoxin microcystin LR and its selection using compe
58 rowth, persistence and the production of the hepatotoxin microcystin, but the physiological mechanism
59 dominance and elevated concentrations of the hepatotoxin microcystin.
60 gal blooms (cyanoHABs) and production of the hepatotoxin, microcystin.
61 of cyclic peptides, including the widespread hepatotoxins microcystins and nodularins.
62                         Among well described hepatotoxins, new reports appeared with highly active an
63  that copper may be acting in synergy with a hepatotoxin, or 2) that there may be a genetic predispos
64 xification and subsequent elimination of the hepatotoxin, over AFB1 exo-8,9-oxidation.
65                                          The hepatotoxin phomopsin A (PHO-A), a secondary metabolite
66              The transport of microcystin, a hepatotoxin produced by cyanobacteria (e.g., Microcystis
67             Microcystins (MCs) are primarily hepatotoxins produced by cyanobacteria and are responsib
68                       Microcystins (MCs) are hepatotoxins produced by cyanobacteria responsible for t
69            Microcystins (MCs) are a group of hepatotoxins produced by cyanobacteria that have not had
70 stins, the highly toxic low-molecular-weight hepatotoxins produced by cyanobacteria.
71 nd INH causes accumulation of the endogenous hepatotoxin protoporphyrin IX in the liver through PXR-m
72 er regeneration, inflammatory bowel disease, hepatotoxin sensitivity, and the diagnostic, persistent
73  against cholestatic liver injury induced by hepatotoxin such as ANIT.
74 ls has been shown to occur after exposure to hepatotoxins such as CCl4.
75 nmentally exposed to cyanobacteria producing hepatotoxins, such as microcystins (MCs), together with
76  and for the hepatocyte apoptosis induced by hepatotoxins that results in liver injury.
77 trasubstituted piperidine A-ring unit of the hepatotoxin was efficiently constructed.
78 astically increased and toxicity of a set of hepatotoxins was detected at clinically relevant concent
79 ter bromobenzene (BB), a model GSH-depleting hepatotoxin, was administered to the Syrian hamster.