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Article ; Online: Alteration of mitochondrial DNA homeostasis in drug-induced liver injury.

Fromenty, Bernard

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

2019 Volume 135, Page(s) 110916

Abstract: Mitochondrial DNA (mtDNA) encodes for 13 proteins involved in the oxidative phosphorylation (OXPHOS) process. In liver, genetic or acquired impairment of mtDNA homeostasis can reduce ATP output but also decrease fatty acid oxidation, thus leading to ... ...

Abstract	Mitochondrial DNA (mtDNA) encodes for 13 proteins involved in the oxidative phosphorylation (OXPHOS) process. In liver, genetic or acquired impairment of mtDNA homeostasis can reduce ATP output but also decrease fatty acid oxidation, thus leading to different hepatic lesions including massive necrosis and microvesicular steatosis. Hence, a severe impairment of mtDNA homeostasis can lead to liver failure and death. An increasing number of investigations report that some drugs can induce mitochondrial dysfunction and drug-induced liver injury (DILI) by altering mtDNA homeostasis. Some drugs such as ciprofloxacin, antiretroviral nucleoside reverse-transcriptase inhibitors and tacrine can inhibit hepatic mtDNA replication, thus inducing mtDNA depletion. Drug-induced reduced mtDNA levels can also be the consequence of reactive oxygen species-mediated oxidative damage to mtDNA, which triggers its degradation by mitochondrial nucleases. Such mechanism is suspected for acetaminophen and troglitazone. Other pharmaceuticals such as linezolid and tetracyclines can impair mtDNA translation, thus selectively reducing the synthesis of the 13 mtDNA-encoded proteins. Lastly, some drugs might alter the mtDNA methylation status but the pathophysiological consequences of such alteration are still unclear. Drug-induced impairment of mtDNA homeostasis is probably under-recognized since preclinical and post-marketing safety studies do not classically investigate mtDNA levels, mitochondrial protein synthesis and mtDNA oxidative damage.
MeSH term(s)	Animals ; Anti-Infective Agents/adverse effects ; Antineoplastic Agents/adverse effects ; Chemical and Drug Induced Liver Injury/metabolism ; DNA Damage/drug effects ; DNA Replication/drug effects ; DNA, Mitochondrial/metabolism ; Homeostasis/physiology ; Humans ; Mitochondria/drug effects ; Protein Biosynthesis/drug effects
Chemical Substances	Anti-Infective Agents ; Antineoplastic Agents ; DNA, Mitochondrial
Language	English
Publishing date	2019-10-25
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2019.110916
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Article ; Online: Letter to the Editor Regarding the Article Rotenone Increases Isoniazid Toxicity but Does Not Cause Significant Liver Injury: Implications for the Hypothesis that Inhibition of the Mitochondrial Electron Transport Chain Is a Common Mechanism of Idiosyncratic Drug-Induced Liver Injury by Cho and Co-Workers, 2019.

Fromenty, Bernard

Chemical research in toxicology

2019 Volume 33, Issue 1, Page(s) 2–4

MeSH term(s)	Chemical and Drug Induced Liver Injury ; Electron Transport ; Humans ; Isoniazid ; Rotenone
Chemical Substances	Rotenone (03L9OT429T) ; Isoniazid (V83O1VOZ8L)
Language	English
Publishing date	2019-12-17
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	639353-6
ISSN	1520-5010 ; 0893-228X
ISSN (online)	1520-5010
ISSN	0893-228X
DOI	10.1021/acs.chemrestox.9b00416
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Article ; Online: Mitochondrial alterations in fatty liver diseases.

Fromenty, Bernard / Roden, Michael

Journal of hepatology

2022 Volume 78, Issue 2, Page(s) 415–429

Abstract: Fatty liver diseases can result from common metabolic diseases, as well as from xenobiotic exposure and excessive alcohol use, all of which have been shown to exert toxic effects on hepatic mitochondrial functionality and dynamics. Invasive or complex ... ...

Abstract	Fatty liver diseases can result from common metabolic diseases, as well as from xenobiotic exposure and excessive alcohol use, all of which have been shown to exert toxic effects on hepatic mitochondrial functionality and dynamics. Invasive or complex methodology limits large-scale investigations of mitochondria in human livers. Nevertheless, abnormal mitochondrial function, such as impaired fatty acid oxidation and oxidative phosphorylation, drives oxidative stress and has been identified as an important feature of human steatohepatitis. On the other hand, hepatic mitochondria can be flexible and adapt to the ambient metabolic condition to prevent triglyceride and lipotoxin accumulation in obesity. Experience from studies on xenobiotics has provided important insights into the regulation of hepatic mitochondria. Increasing awareness of the joint presence of metabolic disease-related (lipotoxic) and alcohol-related liver diseases further highlights the need to better understand their mutual interaction and potentiation in disease progression. Recent clinical studies have assessed the effects of diets or bariatric surgery on hepatic mitochondria, which are also evolving as an interesting therapeutic target in non-alcoholic fatty liver disease. This review summarises the current knowledge on hepatic mitochondria with a focus on fatty liver diseases linked to obesity, type 2 diabetes and xenobiotics.
MeSH term(s)	Humans ; Non-alcoholic Fatty Liver Disease/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Liver/metabolism ; Mitochondria/metabolism ; Obesity/complications ; Obesity/metabolism
Language	English
Publishing date	2022-10-07
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2022.09.020
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Article: Alteration of mitochondrial DNA homeostasis in drug-induced liver injury

Fromenty, Bernard

Food and chemical toxicology. 2020 Jan., v. 135

2020

Abstract	Mitochondrial DNA (mtDNA) encodes for 13 proteins involved in the oxidative phosphorylation (OXPHOS) process. In liver, genetic or acquired impairment of mtDNA homeostasis can reduce ATP output but also decrease fatty acid oxidation, thus leading to different hepatic lesions including massive necrosis and microvesicular steatosis. Hence, a severe impairment of mtDNA homeostasis can lead to liver failure and death. An increasing number of investigations report that some drugs can induce mitochondrial dysfunction and drug-induced liver injury (DILI) by altering mtDNA homeostasis. Some drugs such as ciprofloxacin, antiretroviral nucleoside reverse-transcriptase inhibitors and tacrine can inhibit hepatic mtDNA replication, thus inducing mtDNA depletion. Drug-induced reduced mtDNA levels can also be the consequence of reactive oxygen species-mediated oxidative damage to mtDNA, which triggers its degradation by mitochondrial nucleases. Such mechanism is suspected for acetaminophen and troglitazone. Other pharmaceuticals such as linezolid and tetracyclines can impair mtDNA translation, thus selectively reducing the synthesis of the 13 mtDNA-encoded proteins. Lastly, some drugs might alter the mtDNA methylation status but the pathophysiological consequences of such alteration are still unclear. Drug-induced impairment of mtDNA homeostasis is probably under-recognized since preclinical and post-marketing safety studies do not classically investigate mtDNA levels, mitochondrial protein synthesis and mtDNA oxidative damage.
Keywords	RNA-directed DNA polymerase ; acetaminophen ; adenosine triphosphate ; antiretroviral agents ; beta oxidation ; ciprofloxacin ; death ; enzyme inhibitors ; homeostasis ; linezolid ; liver ; liver failure ; methylation ; mitochondria ; mitochondrial DNA ; necrosis ; nucleases ; nucleosides ; oxidative phosphorylation ; oxygen ; protein synthesis ; proteins ; tetracyclines ; translation (genetics)
Language	English
Dates of publication	2020-01
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2019.110916
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Burn after feeding. An old uncoupler of oxidative phosphorylation is redesigned for the treatment of nonalcoholic fatty liver disease.

Fromenty, B

Clinics and research in hepatology and gastroenterology

2014 Volume 38, Issue 5, Page(s) 545–549

Abstract: Uncoupling of oxidative phosphorylation (OXPHOS) in brown adipose tissue can be used by hibernating animals to produce heat at the expense of their fat mass. In a recent work, Dr Shulman et al. generated a liver-targeted derivative of the prototypical ... ...

Abstract	Uncoupling of oxidative phosphorylation (OXPHOS) in brown adipose tissue can be used by hibernating animals to produce heat at the expense of their fat mass. In a recent work, Dr Shulman et al. generated a liver-targeted derivative of the prototypical OXPHOS uncoupler 2,4-dinitrophenol that alleviated steatosis, hypertriglyceridemia and insulin resistance in several models of nonalcoholic fatty liver disease and type 2 diabetes.
MeSH term(s)	2,4-Dinitrophenol/therapeutic use ; Animals ; Mice ; Non-alcoholic Fatty Liver Disease/drug therapy ; Non-alcoholic Fatty Liver Disease/metabolism ; Oxidative Phosphorylation ; Rats ; Uncoupling Agents/therapeutic use
Chemical Substances	Uncoupling Agents ; 2,4-Dinitrophenol (Q13SKS21MN)
Language	English
Publishing date	2014-10
Publishing country	France
Document type	Journal Article
ZDB-ID	2594333-9
ISSN	2210-741X ; 2210-7401
ISSN (online)	2210-741X
ISSN	2210-7401
DOI	10.1016/j.clinre.2014.04.013
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Xenobiotic-Induced Aggravation of Metabolic-Associated Fatty Liver Disease.

Massart, Julie / Begriche, Karima / Corlu, Anne / Fromenty, Bernard

International journal of molecular sciences

2022 Volume 23, Issue 3

Abstract: Metabolic-associated fatty liver disease (MAFLD), which is often linked to obesity, encompasses a large spectrum of hepatic lesions, including simple fatty liver, steatohepatitis, cirrhosis and hepatocellular carcinoma. Besides nutritional and genetic ... ...

Abstract	Metabolic-associated fatty liver disease (MAFLD), which is often linked to obesity, encompasses a large spectrum of hepatic lesions, including simple fatty liver, steatohepatitis, cirrhosis and hepatocellular carcinoma. Besides nutritional and genetic factors, different xenobiotics such as pharmaceuticals and environmental toxicants are suspected to aggravate MAFLD in obese individuals. More specifically, pre-existing fatty liver or steatohepatitis may worsen, or fatty liver may progress faster to steatohepatitis in treated patients, or exposed individuals. The mechanisms whereby xenobiotics can aggravate MAFLD are still poorly understood and are currently under deep investigations. Nevertheless, previous studies pointed to the role of different metabolic pathways and cellular events such as activation of de novo lipogenesis and mitochondrial dysfunction, mostly associated with reactive oxygen species overproduction. This review presents the available data gathered with some prototypic compounds with a focus on corticosteroids and rosiglitazone for pharmaceuticals as well as bisphenol A and perfluorooctanoic acid for endocrine disruptors. Although not typically considered as a xenobiotic, ethanol is also discussed because its abuse has dire consequences on obese liver.
MeSH term(s)	Humans ; Lipogenesis ; Liver/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Obesity/metabolism ; Xenobiotics/adverse effects ; Xenobiotics/metabolism
Chemical Substances	Xenobiotics
Language	English
Publishing date	2022-01-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23031062
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Article ; Online: Bridging the gap between old and new concepts in drug-induced liver injury.

Fromenty, B

Clinics and research in hepatology and gastroenterology

2013 Volume 37, Issue 1, Page(s) 6–9

Abstract: Recent studies have provided important information in the field of drug-induced liver injury (DILI), in particular regarding the pathogenesis of acetaminophen hepatotoxicity. However, these studies have sometimes left aside some old (but seminal) ... ...

Abstract	Recent studies have provided important information in the field of drug-induced liver injury (DILI), in particular regarding the pathogenesis of acetaminophen hepatotoxicity. However, these studies have sometimes left aside some old (but seminal) findings. Efforts should be made to bridge the gap between old and new concepts in DILI.
MeSH term(s)	Chemical and Drug Induced Liver Injury/etiology ; Humans
Language	English
Publishing date	2013-02
Publishing country	France
Document type	Journal Article
ZDB-ID	2594333-9
ISSN	2210-741X ; 2210-7401
ISSN (online)	2210-741X
ISSN	2210-7401
DOI	10.1016/j.clinre.2012.12.003
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Article ; Online: Fat accretion in a subpopulation of hepatocytes as a strategy to protect the whole liver against oxidative stress and lipotoxicity.

Fromenty, B

Clinics and research in hepatology and gastroenterology

2013 Volume 37, Issue 6, Page(s) 553–555

Abstract: Fatty liver can be induced by obesity, some drugs and alcohol intoxication. In this liver lesion, lipid accumulation can involve only some hepatocytes but the significance of this cell-to-cell heterogeneity is unknown. In a recent work, Dr Pol et al. ... ...

Abstract	Fatty liver can be induced by obesity, some drugs and alcohol intoxication. In this liver lesion, lipid accumulation can involve only some hepatocytes but the significance of this cell-to-cell heterogeneity is unknown. In a recent work, Dr Pol et al. propose that high-fat hepatocytes could protect the cell population against oxidative stress and lipotoxicity.
MeSH term(s)	Animals ; Hepatocytes/cytology ; Lipid Metabolism ; Lipids/chemistry
Chemical Substances	Lipids
Language	English
Publishing date	2013-12
Publishing country	France
Document type	Comment ; Journal Article
ZDB-ID	2594333-9
ISSN	2210-741X ; 2210-7401
ISSN (online)	2210-741X
ISSN	2210-7401
DOI	10.1016/j.clinre.2013.08.005
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Article ; Online: Rôle des acides gras dans l’induction du cytochrome P450 2E1 hépatique : implication dans l’étiologie de la stéatohépatite non alcoolique et dans l’hépatotoxicité du paracétamol

Penhoat, C. / Massart, J. / Fromenty, B. / Begriche, K.

Nutrition clinique et métabolisme. 2023 May, v. 37, no. 2, p. e77-e78

2023

Abstract: ... dans les hépatocytes par le transporteur CD36/FAT et une diminution de la b-oxydation mitochondriale. Les effets ...

Abstract	La stéatose hépatique (non-alcoholic fatty liver [NAFL]) est caractérisée par une accumulation excessive de triglycérides dans le foie et touche aujourd’hui un quart de la population mondiale. Bien que souvent bénigne, la NAFL peut progressivement évoluer vers une stéatohépatite non alcoolique (non-alcoholic steatohepatitis [NASH]), une lésion potentiellement plus grave définie par la présence concomitante d’une NAFL, de lésions nécro-inflammatoires évolutives et d’un ballonnement hépatocytaire. La NASH peut elle-même être à l’origine d’une cirrhose voire d’un carcinome hépatocellulaire. Une meilleure compréhension des mécanismes d’aggravation de la NAFL vers la NASH représente donc un enjeu majeur de santé publique. Plusieurs études ont mis en évidence que le cytochrome P450 2E1 (CYP2E1) pourrait être impliqué dans ces mécanismes d’aggravation. L’induction du CYP2E1 a en effet pour particularité de générer des espèces réactives de l’oxygène (EROs) qui sont sources d’un stress oxydant propice à l’aggravation de la NAFL en NASH. Des travaux ont rapporté le rôle de certains acides gras (AGs) parmi les facteurs métaboliques susceptibles d’activer le CYP2E1, en particulier dans un contexte d’obésité et/ou de NAFL. Outre son rôle potentiel dans l’aggravation de la NAFL en NASH, le CYP2E1 est impliqué dans la toxicité hépatique du paracétamol (PRC), observée généralement après un surdosage (>10g/j) intentionnel ou non, et plus rarement au cours de traitements à des doses pharmacologiques (3–4g/j). Ainsi, le PRC pourrait être plus toxique dans un contexte de NAFL et d’obésité. Afin d’identifier plus précisément l’impact de différents AGs sur l’induction du CYP2E1, la NAFL et sur la toxicité du PRC, la lignée d’hépatocarcinome humain HepaRG a été utilisée. Ces cellules ont été traitées pendant une semaine par neuf AGs différents (150μM). Un traitement par le PRC (10 ou 20mM) pendant les 24 dernières heures a également été réalisé. L’activité du CYP2E1 a été significativement induite par les AGs palmitique (PA), stéarique (SA) et linoléique (LA) dans notre modèle. Pour le PA et le SA, les mécanismes impliqués passeraient par une augmentation de la stabilité de la protéine CYP2E1. Concernant la NAFL, uniquement le LA a favorisé une accumulation significative de triglycérides intracellulaires ainsi que l’expression de certains gènes représentatifs des gouttelettes lipidiques. Pour cet AG, l’accumulation des triglycérides pourrait s’expliquer par une augmentation de l’entrée des AGs dans les hépatocytes par le transporteur CD36/FAT et une diminution de la b-oxydation mitochondriale. Les effets de ces trois AGs sur le stress oxydant, le stress du réticulum endoplasmique et la fonction mitochondriale ont ensuite été évalués. Après une semaine de traitement, aucune variation de stress cellulaire n’a été mesurée. En revanche, une diminution de la respiration maximale a été observée en réponse aux AGs PA et SA. Enfin, une potentialisation de la toxicité du PRC a été observée avec les AGs PA et SA mais pas avec le LA. Le stress oxydant a ensuite été évalué au vu de son importance dans l’hépatotoxicité du PRC. Une potentialisation de la production d’EROs ainsi qu’une altération de la réponse antioxydante ont été mises en évidence avec les AGs PA et SA. Trois AGs inducteurs du CYP2E1 (c.-à-d. PA, SA et LA) ont été identifiés. De façon intéressante, ces AGs n’ont pas tous le même impact sur la NAFL dans nos conditions expérimentales puisque seul le LA entraînait une stéatose. En effet, le métabolisme lipidique hépatocytaire s’effectue de manière différente selon le traitement en AG. De plus, une potentialisation de la toxicité du PRC avec les AGs PA et SA et un stress oxydant avec ces deux AGs ont également été mis en évidence. Ainsi, la sensibilité accrue à l’hépatotoxicité du PRC dans un contexte de nutrition hyperlipidique et de NAFL pourrait en partie être expliquée par l’induction du CYP2E1, qui cependant peut s’observer expérimentalement de façon indépendante de l’accumulation des triglycérides intracellulaires.
Keywords	cytochrome P-450 ; fatty liver ; nutrition
Language	English
Dates of publication	2023-05
Size	p. e77-e78
Publishing place	Elsevier Masson SAS
Document type	Article ; Online
ZDB-ID	1131758-9
ISSN	0985-0562
ISSN	0985-0562
DOI	10.1016/j.nupar.2023.03.142
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Busulfan induces steatosis in HepaRG cells but not in primary human hepatocytes: Possible explanations and implication for the prediction of drug-induced liver injury.

Allard, Julien / Bucher, Simon / Ferron, Pierre-Jean / Launay, Youenn / Fromenty, Bernard

Fundamental & clinical pharmacology

2023 Volume 38, Issue 1, Page(s) 152–167

Abstract: Background: The antineoplastic drug busulfan can induce different hepatic lesions including cholestasis and sinusoidal obstruction syndrome. However, hepatic steatosis has never been reported in patients.: Objectives: This study aimed to determine ... ...

Abstract	Background: The antineoplastic drug busulfan can induce different hepatic lesions including cholestasis and sinusoidal obstruction syndrome. However, hepatic steatosis has never been reported in patients. Objectives: This study aimed to determine whether busulfan could induce steatosis in primary human hepatocytes (PHH) and differentiated HepaRG cells. Methods: Neutral lipids were determined in PHH and HepaRG cells. Mechanistic investigations were performed in HepaRG cells by measuring metabolic fluxes linked to lipid homeostasis, reduced glutathione (GSH) levels, and expression of genes involved in lipid metabolism and endoplasmic reticulum (ER) stress. Analysis of two previous transcriptomic datasets was carried out. Results: Busulfan induced lipid accumulation in HepaRG cells but not in six different batches of PHH. In HepaRG cells, busulfan impaired VLDL secretion, increased fatty acid uptake, and induced ER stress. Transcriptomic data analysis and decreased GSH levels suggested that busulfan-induced steatosis might be linked to the high expression of glutathione S-transferase (GST) isoenzyme A1, which is responsible for the formation of the hepatotoxic sulfonium cation conjugate. In keeping with this, the GST inhibitor ethacrynic acid and the chemical chaperone tauroursodeoxycholic acid alleviated busulfan-induced lipid accumulation in HepaRG cells supporting the role of the sulfonium cation conjugate and ER stress in steatosis. Conclusion: While the HepaRG cell line is an invaluable tool for pharmacotoxicological studies, it might not be always an appropriate model to predict and mechanistically investigate drug-induced liver injury. Hence, we recommend carrying out toxicological investigations in both HepaRG cells and PHH to avoid drawing wrong conclusions on the potential hepatotoxicity of drugs and other xenobiotics.
MeSH term(s)	Humans ; Busulfan/toxicity ; Busulfan/metabolism ; Hepatocytes/metabolism ; Fatty Liver/chemically induced ; Fatty Liver/metabolism ; Chemical and Drug Induced Liver Injury/etiology ; Drug-Related Side Effects and Adverse Reactions ; Cations/metabolism ; Lipids/adverse effects ; Liver/metabolism
Chemical Substances	Busulfan (G1LN9045DK) ; Cations ; Lipids
Language	English
Publishing date	2023-09-04
Publishing country	England
Document type	Journal Article
ZDB-ID	639134-5
ISSN	1472-8206 ; 0767-3981
ISSN (online)	1472-8206
ISSN	0767-3981
DOI	10.1111/fcp.12951
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