Role of temperature on protein and mRNA cytochrome P450 3A (CYP3A) isozymes expression and midazolam oxidation by cultured rat precision-cut liver slices

Rekka, Eleni A.; Евдокимова, Е. В.; Eeckhoudt, Stéphane; Labar, Geoffray; Calderón, Pedro Buc

doi:10.1016/s0006-2952(02)01258-3

Cited by 22 publications

(10 citation statements)

References 39 publications

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“…Human CYP3A4 and rat CYP3A1 (CYP3A23) proteins have 73% homology (Lewis, 1996). It has been reported that CYP3A1 (CYP3A23) (Mahnke et al, 1997) or CYP3A2 (Debri et al, 1995;Hoen et al, 2001;Rekka et al, 2002) is the major CYP3A protein in rats. Hence, the role of CYP3A23 and CYP3A2 on the formation dmd.aspetjournals.org of OH-CZX in rats was measured by treatment with DDT (an inducer of CYP3A2; Sierra-Santoyo et al, 2000) or DDE (an inducer of CYP3A23; You et al, 1999).…”

Section: Pharmacokinetics Of Czx In Rats With U-arfmentioning

confidence: 99%

Effects of Acute Renal Failure on the Pharmacokinetics of Chlorzoxazone in Rats

Moon¹,

Lee²,

Chung³

et al. 2003

Drug Metab Dispos

111

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ABSTRACT:The purpose of this study is to report the changes of CYP2E1, CYP1A2, CYP2B1/2, CYP2C11, CYP3A23, and CYP3A2 expression and pharmacokinetics and tissue distribution of chlorzoxazone (CZX) and 6-hydroxychlorzoxazone (OH-CZX) in rats with acute renal failure induced by uranyl nitrate (U-ARF), and the role of CYP3A23 and CYP3A2 in the formation of OH-CZX in rats with U-ARF. In rats with U-ARF, CYP2C11 decreased to 20% of control, whereas CYP2E1 and CYP3A23 increased 2.3 and 4 times, respectively, compared with control. But expression of CYP1A2 and CYP2B1/2 was not changed by U-ARF. After i.v. administration of CZX at a dose of 20 mg/kg to rats with U-ARF, the areas under the plasma concentration-time curve from time 0 to time infinity (AUCs) of CZX and OH-CZX were significantly smaller and greater, respectively, than those in control rats. In rats with U-ARF, CZX was below the detection limit at 120 min in all rat tissues studied, whereas it was detected in all tissues of control rats at both 30 and 120 min. However, in control rats, OH-CZX was below the detection limit at both 30 and 120 min in all rat tissues except kidney, whereas it was detected in all tissues of rats with U-ARF at both 30 and 120 min. Based on results from supporting experiments with DDT and 2,2-bis(4-chlorophenyl)1,1-dichloroethylene treatment of rats, the contribution of CYP3A23 and CYP3A2 to the enhanced formation of OH-CZX in rats with U-ARF is likely to be negligible.

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Section: Pharmacokinetics Of Czx In Rats With U-arfmentioning

confidence: 99%

Effects of Acute Renal Failure on the Pharmacokinetics of Chlorzoxazone in Rats

Moon¹,

Lee²,

Chung³

et al. 2003

Drug Metab Dispos

111

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“…Physiological and biochemical changes may happen during hypothermia therapy related to a reduction in blood flow 13) and energy deficiency. 14) Therefore, pharmacokinetics of a drug during hypothermia should differ largely from normothermic conditions. There have been a few reports that recently investigated the influence of hypothermia on drug pharmacokinetics and pharmacodynamics such as phenytoin, 15) neostigmine 16) and vecuronium.…”

mentioning

confidence: 99%

Change in Pharmacokinetics of Model Compounds with Different Elimination Processes in Rats during Hypothermia

Nishida

Okazaki

Sakamoto

et al. 2007

Biological & Pharmaceutical Bulletin

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Cerebral ischemia accompanied by head trauma, cerebral and cardiac infarction leads to neuron dysfunction and cell death, 1) and its after-effects such as dementia, perception injury and hemiplegia are serious problems. Excess glutamate released from the neuron, energy disorder from impaired circulation and free radical generation have been clarified as the causes leading to neuron death involved with cerebral ischemia.2,3) Busto et al. reported in 1989 4) that it was possible to prevent neuron dysfunction and cell death in the ischemia by lowering the body temperature of the rats, i.e. surface cooling to 32-33°C. The multiple mechanisms of hypothermia-induced neuroprotection were identified such as reduction in cerebral metabolism, energy depletion and stabilization of cell membranes as reported previously.4-10) Hypothermia therapy has been increasingly applied to the humans 11) since it was proved useful in rats and dogs to treat experimental ischemic brain injury in the early 1990s.On the other hand, hypothermia therapy possibly causes side effects such as arrhythmia, impaired immune function and coagulation disorders as reviewed by Schubert.12) In order to negate these side effects, several kinds of medicines such as antiarrhythmic drugs, antibiotics and anticoagulants are administered to the patients. 12) Moreover, like other critically ill patients, those with severe head injuries typically receive a large number of medications. In addition, although combination pharmacotherapy with an inhibitor of glutamate and calcium might act synergistically by attenuating an ischemia-induced release of neurotoxic glutamate, 2,3) it is possible for undesirable drug-interactions to occur. Although hypothermic patients tend to receive many different pharmacologic agents, most of them are administered according to dosing schedules derived from the normothermic host. These schedules do not take into consideration any changes in drug pharmacokinetics or pharmacodynamics associated with hypothermia therapy. Physiological and biochemical changes may happen during hypothermia therapy related to a reduction in blood flow 13) and energy deficiency. 14) Therefore, pharmacokinetics of a drug during hypothermia should differ largely from normothermic conditions. There have been a few reports that recently investigated the influence of hypothermia on drug pharmacokinetics and pharmacodynamics such as phenytoin, 15) neostigmine 16) and vecuronium. 17) As well, the possibility of side effects and drug-interactions caused by variations in drug pharmacokinetics during hypothermia must be sufficiently understood.In the present study, we assessed systematically the influence of hypothermia at 32°C on the pharmacokinetics of several compounds as models with different elimination processes. Moreover, we examined the pharmacokinetic change in hypothermia at 28°C, aiming to consider the unexpected conditions such as too much cooling and body temperature dependency on pharmacokinetic change of a drug in the patients fully by three different ...

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“…The dimethylaminohydrazonofurylquinones 1-3 employed in this study were prepared by oxidative coupling reactions of 2-furaldehyde N,N-dimethylhydrazone with 1,4-naphthoquinone, 2-chloro-1,4-naphthoquinone and 2-methoxy-1,4-benzoquinone in acetic acid according to a previously reported procedure [17]. The aldehydes 4-6 were obtained by acid-induced hydrolysis of compounds 1-3 under mild conditions ( Fig.…”

Section: Chemical Synthesismentioning

confidence: 99%

“…The first model (TLT cells) has been widely used to assess both in vivo and in vitro cytotoxic anticancer effects [12][13][14], facilitating the investigation of possible mechanisms involved in cancer cell death. The second method, PCLS, is a suitable model for studying the toxic effects of xenobiotics on healthy tissues at both molecular and cell biology levels [15][16][17][18]. The end points for assessing the biological reactivity of furylquinones in TLT cells were LDH leakage (index of cell survival), the intracellular content of reduced glutathione (GSH) and ATP (indexes of cell metabolism which are more sensitive to LDH leakage), and caspase-3 activity (type of cell death).…”

Section: Introductionmentioning

confidence: 99%

An in vitro comparative study with furyl-1,4-quinones endowed with anticancer activities

et al. 2010

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We describe the biological activity of some furylbenzo- and naphthoquinones (furylquinones) on hepatocarcinoma cells and healthy rat liver slices. The effects of furylquinones on cancer cells (Transplantable Liver Tumor, TLT) were assessed by measuring cell death (membrane cell lysis); intracellular contents of ATP and GSH and the activity of caspase-3 were used to determine the type of cell death. Most of the furylquinones tested (at a concentration of 25 μg/ml) induced caspase-independent cell death but compound 4 had no cytotoxic effects. The levels of both ATP and GSH were severely affected by quinones 1, 2 and 5, while no effect was observed with compound 4. These cytotoxic properties of quinones are associated with physico-chemical properties as shown by the LUMO energies and lipophilicity. Interestingly, no cytotoxic effects of furylquinones were detected when the in vitro model of precision-cut liver slices (PCLS) was used. Indeed, although CYP2E1 activity was slightly affected, ATP and GSH levels as well as protein synthesis were not modified by furylquinones. Paracetamol, a well-known hepatotoxicant, reduced these parameters by more than 80% compared to control conditions. Taking into account the considerable incidence of adverse-effects induced by most current anticancer drugs, the selective cytotoxicity shown by compounds 1, 2 and 5, in particular that of 1, represents a safety factor that encourages the further development of these quinones as new drugs in cancer therapy.

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Role of temperature on protein and mRNA cytochrome P450 3A (CYP3A) isozymes expression and midazolam oxidation by cultured rat precision-cut liver slices

Cited by 22 publications

References 39 publications

Effects of Acute Renal Failure on the Pharmacokinetics of Chlorzoxazone in Rats

Effects of Acute Renal Failure on the Pharmacokinetics of Chlorzoxazone in Rats

Change in Pharmacokinetics of Model Compounds with Different Elimination Processes in Rats during Hypothermia

An in vitro comparative study with furyl-1,4-quinones endowed with anticancer activities

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