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J K Chipman

Publications and source records attributed to J K Chipman.

At least 19 recordsLinked to original sources
PubMed2006

Substrate characterisation of a recombinant sulfotransferase SULT1 and mRNA expression in chub (Leuciscus cephalus) tissues.

We have studied the role and regulation of sulfonation of xenobiotics and endogenous substrates in Leuciscus cephalus, an abundant and environmentally relevant freshwater fish. A sulfotransferase 1 (SULT1) cDNA and promoter region was cloned from chub liver and the cDNA expressed in Escherichia coli. The translated protein displayed 51% and 50% amino acid identity to mSULT1D1, hSULT1A1, respectively. We identified two conserved co-substrate binding motifs for 3'-phosphoadenosine 5'-phosphosulfate: RKGxxGDWKxxFT and YPKSGTxW. The recombinant SULT displayed a strong preference towards the isoflavones genistein (K(m)=1.7 microM) and daidzein (K(m)=4.4 microM) and lesser activity towards the endogenous substrate dopamine. Based on sequence identity and substrate preferences, the SULT was classified as SULT1,3. SULT1,3 mRNA expression was highest in the liver and kidney with low levels expressed in brain, gonad, and gill. Mature males displayed higher hepatic SULT1,3 mRNA expression compared to females. Analysis of the promoter region revealed several putative half palindromic estrogen response elements (ERE).

Amino Acid Sequence↗
PubMed2006

Activity of OGG1 variants in the repair of pro-oxidant-induced 8-oxo-2'-deoxyguanosine.

Cells are continuously exposed to damaging reactive oxygen species (ROS), which are produced from both endogenous and exogenous sources. 8-Oxodeoxyguanosine (8-oxodG) is an abundant base lesion formed during oxidative stress which, if not repaired, can give rise to G:C-->T:A transversions in DNA. The 8-oxoguanine DNA glycosylase-1 (OGG1)-initiated base excision repair (BER) pathway operates to remove 8-oxodG lesions. Ogg1 deletion and polymorphism may result in a hypermutator phenotype and susceptibility to oxidative pathologies including cancer. Limited and conflicting evidence exists regarding the repair capacity of a prevalent human OGG1 (hOGG1) polymorphism, the Cys326-hOGG1 variant. The formamidopyrimidine DNA glycosylase (FPG)-modified comet assay was used to investigate the ability of sodium dichromate, potassium bromate and Ro19-8022 (+light) to induce DNA damage in mogg1(-/-) null (KO) and wild-type (WT) mouse embryonic fibroblasts (MEFs) and to assess hOGG1 variant-initiated BER capacities under conditions of oxidative stress. Treatment of WT MEFs with these pro-oxidant agents induced direct DNA strand breaks in a concentration-dependent manner, whereas, identical treatment of KO MEFs produced no effect. In contrast, KO MEFs accumulated significantly more FPG-sensitive sites than WT MEFs. Expression of hOGG1 in KO MEFs restored the WT phenotype in response to all pro-oxidants tested. The results suggest OGG1-initiated BER generates direct DNA strand breaks detected by the conventional comet assay, thus it is important that researchers do not interpret these as direct damage per se but rather a reflection of the repair process. The data also indicate Cys326-hOGG1-initiated BER is transiently impaired with respect to Ser326-hOGG1 (wild-type)- and Gly326-hOGG1 (artificial)-initiated BER following pro-oxidant treatment, possibly via hOGG1 cysteine 326 oxidation. This finding suggests the homozygous cys326/cys326 genotype may be classified as a biomarker of disease susceptibility, which is in support of a growing body of epidemiological evidence.

Animals↗
PubMed2006

Oxidative damage produced by Cr(VI) and repair in mussel (Mytilus edulis L.) gill.

This study has assessed DNA damage induced by oxidative stress and its subsequent repair in mussels. Gill was obtained from mussels collected from New Brighton, UK within 24 h and also after 1 month maintenance under laboratory conditions. The pro-oxidant sodium dichromate produced a statistically significant increase in DNA strand breaks (DSB) in these gill cells at both time points as measured by the COMET assay. The response was higher at 1 month in association with a higher concentration of GSH which is known to activate Cr(VI) producing reactive oxygen species. DSB were shown, through studies in wild type and OGG-1-null mouse fibroblasts, to be produced by repair enzymes in response to Cr(VI). In support of evidence for repair of oxidative DNA damage, we have also demonstrated for the first time repair activity in mussel gill towards 8-oxo-dG using an oligonucleotide cutting assay.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2006

The multiple influences of glutathione on bromate genotoxicity: implications for the dose-response relationship.

Glutathione displays multiple roles in the oxidative genotoxicity of potassium bromate. On the one hand, reduced glutathione has a demonstrated role in the activation of bromate to species capable of oxidising DNA. However, if this activation should occur within the gut or extracellularly once bromate is absorbed, this may limit the ability of the chemical to oxidise cellular DNA in vivo. Moreover, glutathione may offer protection against the damaging species produced by its interaction with bromate. Finally, if bromate exposure of cells is sufficiently high to deplete glutathione, a secondary oxidative stress and associated DNA damage may occur. These observations would suggest non-linearity in the dose-response to DNA damage in vivo.

Animals↗
PubMed2004

Seasonal variation in cytochrome P450 immunopositive protein levels, lipid peroxidation and genetic toxicity in digestive gland of the mussel Mytilus edulis.

The relationship between cytochrome P450 1A- and 2E-immunopositive proteins, lipid peroxidation and DNA strand breaks (SBs) was studied in Mytilus edulis digestive gland at different seasons and at different sites around the UK coast. Cytochrome P4501A (CYP1A)-immunopositive protein and DNA strand breaks were generally lowest in December but there was no correlation between PAH exposure (indicated by chemical measurement and CYP1A-immunopositive protein expression) and DNA strand breaks which was highest at the relatively non-polluted site (Port Quin). As with CYP1A, CYP2E1-immunopositive protein was maximal at most sites in May. Lipid peroxidation, in contrast, did not alter markedly throughout the year. In conclusion, DNA strand breakage was not correlated with any of the above parameters although it did correlate with "scope for growth" as did the inverse of PAH levels. The study highlights the need to establish the relative contribution of DNA damage and DNA repair processes to the production of DNA strand breaks and emphasises the need to consider seasonal variation in interpretation of biomarkers.

Animals↗
PubMed2004

Activation of c-Jun N-terminal kinase in A549 lung carcinoma cells by sodium dichromate: role of dissociation of apoptosis signal regulating kinase-1 from its physiological inhibitor thioredoxin.

Changes in the components of the Jun N-terminal kinase (JNK) signalling pathway were investigated in human A549 lung carcinoma cells treated with sodium dichromate. Sodium dichromate (100 microM, 0-6h) failed to activate nuclear factor kappa B (NF-kappaB) as determined by a lack of nuclear translocation of p65 but resulted in Jun N-terminal kinase activation as assessed by phospho-Jun N-terminal kinase Western blotting in a dose-dependent (>25 microM) and time-dependent (>1h) manner. In addition, c-Jun, a downstream target of Jun N-terminal kinase signalling was also activated with a similar dose- and time-dependency at the level of both protein expression and degree of phosphorylation. In contrast, sodium dichromate treatment had no effect on levels of phospho-p38. Immunoprecipitation demonstrated that apoptosis signal regulating kinase-1 (ASK-1), an upstream activator of Jun N-terminal kinase was dissociated from its inhibitory partner thioredoxin (Trx) in response to sodium dichromate (100 microM, 4h) treatment. This treatment was also associated with a transient (2h) increase in cytosolic levels of thioredoxin but no nuclear translocation of thioredoxin was observed. In conclusion, sodium dichromate had a stimulatory effect on the Jun N-terminal kinase signalling pathway in A549 cells, resulting in activation of downstream effector molecules. We hypothesise that dissociation of apoptosis signal regulating kinase-1 from thioredoxin may be at least partially responsible for Jun N-terminal kinase activation.

Cell Nucleus↗
PubMed2004

Gap junction communication dynamics and bystander effects from ultrasoft X-rays.

Gap junctions provide a route for small molecules to pass directly between cells. Toxic species may spread through junctions into 'bystander' cells, which may be exploited in chemotherapy and radiotherapy. However, this may be prevented by junction closure, and therefore an understanding of the dose-dependency of inhibition of communication and bystander effects is important. Low-energy ionising radiation (ultrasoft X-rays) provides a tool for the study of bystander effects because the area of exposure may be carefully controlled, and thus target cells may be clearly defined. Loss of gap junction-mediated intercellular communication between irradiated cells was dose-dependent, indicating that closure of junctions is proportional to dose. Closure was associated with hyperphosphorylation of connexin43. Inhibition of communication occurred in bystander cells but was not proportional to dose. Inhibition of communication at higher radiation doses may restrict the spread of inhibitory factors, thus protecting bystander cells. The reduction in communication that takes place in bystander cells was dependent on cells being in physical contact, and not on the release of signalling factors into the medium.

Animals↗
PubMed2003

A DNA expression array to detect toxic stress response in European flounder (Platichthys flesus).

As a first stage in developing a DNA array-based approach to investigating the effects of pollutants on an environmentally relevant European fish species, we have constructed a 160-gene custom microarray for European flounder. Degenerate primers were used to amplify 110 different fragments of stress-related and other genes from European flounder cDNA and genomic DNA. Additionally, 22 fragments were obtained by suppressive subtractive hybridisation (SSH). These fragments were cloned and sequenced, then, with additional control genes, used to create a cDNA microarray for flounder. After optimisation of the arraying process, hepatic mRNA was isolated from flounder caught in the polluted Tyne and relatively unpolluted Alde estuaries. Fluorescent cDNA probes were synthesised from the mRNA and used in dual-colour hybridisations to the microarray. A number of transcripts were differentially expressed between Tyne and Alde female flounder but these changes were not significant, due to high inter-individual variation. However, in comparisons between Tyne and Alde male flounder, 11 transcripts were found to significantly differ in expression (P<0.05). Seven transcripts were more highly expressed in the Tyne male fish (CYP1A, UDPGT, alpha-2HS-glycoprotein, dihydropyrimidine dehydrogenase, Cu/Zn SOD, aldehyde dehydrogenase and paraoxonase). Four transcripts (Elongation factor 1 (EF1), EF2, Int-6 and complement component C3) were found to be significantly less abundant in the Tyne male fish. Selected genes were assayed by real-time PCR, then normalised to alpha-tubulin. These assays confirmed the significance of the array results for CYP1A, UDPGT and EF1, but not for Cu/Zn SOD. This study provides a link between traditional single-gene biomarker studies and the emerging field of eco-toxicogenomics, demonstrating the utility of microarray studies on environmentally sampled, non-model organisms.

Animals↗
PubMed2003

Characterisation of the connexin32 promoter and changes in response element complexes in rat liver and hepatocytes during culture associated with oxidative stress.

Hepatic gap junctional intercellular communication (GJIC), mediated principally by connexin 32, provides a mechanism for regulating multicellular activities between neighbouring cells. The control of Cx32 gene expression at the transcriptional level has been investigated in rat liver tissue and in primary rat hepatocytes during culture. Several response elements have been identified and characterised using the electrophoretic mobility shift assay. Nuclear protein extract prepared from rat primary hepatocytes cultured for 2 h gave a larger number of DNA-protein complexes than observed with extracts from liver in vivo, including complexes containing Sp1. In contrast, nuclear extracts prepared from primary rat hepatocytes cultured for 96 h, and subject to oxidative stress, gave altered DNA-protein complexes when compared to those from hepatocytes cultured for 2 h. These results indicate that culture conditions, known to cause a loss of connexin expression, can modulate the transcription of Cx32 in hepatocytes by affecting the regulatory trans/cis-interactions of redox-sensitive zinc finger proteins within the promoter.

Animals↗
PubMed2002

Down-regulation of the DNA-repair endonuclease 8-oxo-guanine DNA glycosylase 1 (hOGG1) by sodium dichromate in cultured human A549 lung carcinoma cells.

Hexavalent chromium is a genotoxic human pulmonary carcinogen that elevates DNA oxidation, apparently through the generation of reactive DNA-damaging intermediates including Cr(V), Cr(IV) and reactive oxygen species. We tested the hypothesis that elevation of DNA oxidation may also be through inhibition of the expression of the repair glycosylase for 8-oxo deoxyguanine (hOGG1) in cultured A549 human lung epithelial cells. Treatment with sodium dichromate (0-100 microM, 16 h) resulted in a concentration-dependent decrease in the levels of OGG1 mRNA as measured by both RT-PCR and RNase protection assay. Sodium dichromate at 25 microM and above gave a marked reduction of OGG1 mRNA expression which was not seen at 1 microM and below. No effect on the expression of the apurinic endonuclease hAPE or the house-keeping gene GAPDH was observed at any of the concentrations of sodium dichromate investigated. Treatment of cells with the pro-oxidant H(2)O(2) (0-200 microM) for 16 h had no detectable effect on the levels of OGG1 mRNA or protein expression suggesting that the effect of sodium dichromate is not mediated by H(2)O(2). Western blotting demonstrated that sodium dichromate (100 microM; 16 h and >25 microM; 28 h) markedly reduced levels of OGG1 protein in nuclear cell extracts. Additionally, treatment of cells with sodium dichromate (>25 microM, 28 h) resulted in a concentration-dependent decrease in the ability of nuclear extracts to nick a synthetic oligonucleotide containing 8-oxo deoxyguanine (8-oxo dG). We conclude that the elevation of 8-oxo dG levels observed in A549 cells treated with sodium dichromate may be, at least in part, due to a reduced capacity to repair endogenous and hexavalent chromium-induced 8-oxo dG.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2002

Flavonoids inhibit genetic toxicity produced by carcinogens in cells expressing CYP1A2 and CYP1A1.

The effects of the flavonoids quercetin, apigenin and chrysin (10 microM) on the genetic toxicity of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and benzo[a]pyrene (BaP) was investigated at sub-cytotoxic concentrations in Chinese hamster V79 cells expressing human or rat cytochromes P450. In V79 r1A2-NH and V79 h1A1-MZ cells, none of the flavonoids increased DNA strand breaks (SB) (measured by the Comet assay) or produced detectable DNA adducts (measured by 32P-post-labelling). Neither IQ nor BaP produced DNA damage in the absence of expressed CYP1A2 or CYP1A1, respectively. DNA damage measured as SB and DNA adducts was detectable in V79 r1A2-NH cells expressing rat CYP1A2 when treated with IQ (2.5-50 microM) and this was inhibited by quercetin. Likewise, DNA damage (SB and DNA adducts) was elevated in V79 h1A1-MZ cells expressing human CYP1A1 when treated with BaP (0.1-0.5 microM) and this was inhibited by chrysin and apigenin, but not by quercetin. The specificity of CYP1A1 inhibition by chrysin and apigenin and CYP1A2 inhibition by quercetin was confirmed by ethylresorufin O-deethylase assay.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed2001

Structure, expression and activation of fish ras genes.

Ras genes encode proteins that play a central role in cell growth signaling cascades. The fish ras genes characterized to date, have a high degree of nucleotide sequence and deduced amino acid similarity with the mammalian ras gene counterparts. A large proportion and wide variety of mammalian tumors possess mutant forms of ras. In such cases, the localization of ras mutations has been restricted to exons I and II, and to codons 12, 13 and 61. Experimental exposure of fish to a range of genotoxic compounds has similarly led to the production of a ras mutational profile for selected species. The inducing compound, tissue investigated and the fish species studied affect the ras mutational spectrum and incidence observed, despite the apparent conserved sequence homology. Furthermore, the fish ras mutational profile differs from that observed in rodent models, including a novel codon (16) mutation. The role of ras genes in tumor formation in feral fish has been investigated using several species collected from areas of high hydrocarbon contamination. Tomcod (Microgadus tomcod), winter flounder (Pseudopleuronectes americanus) and dragonet (Callionymus lyra) liver samples display evidence of ras gene mutations, though for the latter species the codon affected is not characteristic of ras gene mutational profiles. English sole (Pleuronectes vetulus) and European flounder (Platichthys flesus) liver tumor samples so far examined, on the other hand, do not display ras gene mutations. Thus, the pattern and incidence of ras gene mutations in environmentally-induced tumors also appear to be species specific. In determining the basis of both the species susceptibility observed in the field and species differences in effects of laboratory controlled exposures, the interaction of fish ras genes with other components of the cell growth signaling cascade (such as protein kinase C, additional oncogenes and tumor suppressor genes) are discussed. The effect of promoting agents following contaminant-induced initiation could similarly provide answers in unraveling the question of species susceptibility.

Amino Acid Sequence↗
PubMed2001

Induction of DNA-strand breaks in human peripheral blood lymphocytes and A549 lung cells by sodium dichromate: association with 8-oxo-2-deoxyguanosine formation and inter-individual variability.

Hexavalent chromium [Cr(VI)] is a genotoxic carcinogen for which inhalation is a major potential route of exposure in occupational settings. In the present study, the ability of sodium dichromate to cause DNA strand breaks in three populations of cells, human whole blood cells, isolated human peripheral blood lymphocytes and cultured A549 lung epithelial cells, was investigated. Treatment with non-cytotoxic concentrations of sodium dichromate (for 1 h) resulted in a concentration-dependent increase in the number of DNA strand breaks as measured by the Comet assay. The lowest concentrations of sodium dichromate that resulted in a statistically significant (P < 0.01) increase in the number of DNA strand breaks were 500, 50 and 10 microM, respectively, in these cells. The use of formamidopyrimidine glycosylase increased the sensitivity of detection of strand breaks in A549 cells 10-fold, suggesting a role for DNA base oxidation in the mechanism of dichromate-induced DNA strand breaks. In support of this hypothesis, immunocytochemistry indicated an elevation of 8-oxodeoxyguanosine in A549 cells treated with 10 and 500 microM sodium dichromate for 1 h. We also demonstrated 2.11- and 2.5-fold ranges in the level of control and dichromate (500 microM)-induced DNA strand breaks, respectively, in cells of whole blood within a group of healthy volunteers (n = 26). A statistically significant (P < 0.001) positive Pearson's correlation (r = 0.606) was found between control and treated levels of DNA strand breaks, suggesting that factors responsible for relatively low levels of DNA strand breaks in untreated PBL may also offer protection against the formation of dichromate-induced DNA strand breaks.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2000

Nmethyl-N-nitrosourea (MNU) induces papillary thyroid tumours which lack ras gene mutations in the hermaphroditic fish Rivulus marmoratus.

To investigate the patterns of alkylating agent-induced tumour formation, 40 fish (Rivulus marmoratus) were exposed to N-methyl-N-nitrosourea (MNU) at 50 ppm in 10 mM Hepes-buffered synthetic seawater for 2 h. Tumour incidence 4 months after exposure was approximately 95%, and mainly papillary thyroid tumours were induced. For elucidating the molecular event in Rivulus papillary thyroid carcinogenesis, we first analysed for ras gene mutations based on the known ability of MNU to induce point mutations. The amplified R. Marmoratus Ha-and Ki-ras gene exon 1 and 2 regions were checked along with confirming the presence and expression patterns of the DNA repair gene O(6)-methylguanine alkyltransferase (O(6)-MT) and other oncogenes (c-src, c-fos, and c-myc). Ha- and Ki-ras genes from 38 tumour samples were tested for point mutations with direct sequencing but were not found to contain mutations. In this report, based on the lack of Ha- and Ki-ras gene mutations in papillary thyroid tumour induction in R. Marmoratus, we suggest that Ha- and Ki-ras gene-independent pathways such as ret/PTC rearrangements and other activations are involved in Rivulus papillary thyroid carcinogenesis. Teratogenesis Carcinog. Mutagen. 20:1-9, 2000.

Alkylating Agents↗
PubMed2000

Potentiation of epidermal growth factor-induced DNA synthesis in rat hepatocytes by phenobarbitone: possible involvement of oxidative stress and kinase activation.

A transient induction of S phase DNA synthesis is a common feature of non-genotoxic rodent hepatocarcinogens when administered in vivo. In the present study the ability of phenobarbitone (PB) to induce S phase DNA synthesis in primary cultures of rat hepatocytes was investigated. In the absence of serum or growth factors PB was not a mitogen per se. However, stimulation of S phase DNA synthesis by epidermal growth factor (EGF) was enhanced by co-culture with PB. This effect was both time and concentration dependent. The lowest concentration of PB that significantly enhanced the effect of EGF was 10 microM and the effect was maximal at 1.0 mM. At a concentration of 2.0 mM PB no longer enhanced EGF-induced S phase DNA synthesis. Hepatocyte cultures pretreated with PB (0.1 mM) for 2 days were more responsive to the induction of S phase DNA synthesis by EGF for the subsequent 2 days. Despite the inhibition of PB enhancement of S phase DNA synthesis by the antioxidant dimethylthiourea, reduced glutathione was not depleted by PB treatment nor were oxidized glutathione or lipid peroxides elevated. Western blotting analysis showed that PB had no effect on epidermal growth factor receptor (EGFR) autophosphorylation per se after 1 and 48 h culture, enhanced sensitization of EGFR therefore does not appear to contribute to the enhancement of S phase DNA synthesis by PB. In contrast, treatment of hepatocytes with PB for 12 h resulted in a small but statistically significant activation of p42/44 MAP kinase activity and activation of protein kinase C, as measured by redistribution of enzyme activity from a soluble to a particulate compartment of hepatocytes. Therefore, PB-mediated changes in protein kinase activity may contribute to the potentiation this compound affords.

Animals↗
PubMed2000

The role of glutathione in DNA damage by potassium bromate in vitro.

We have investigated the role of reduced glutathione (GSH) in the genetic toxicity of the rodent renal carcinogen potassium bromate (KBrO(3)). A statistically significant increase in the concentration of 8-oxodeoxyguanosine (8-oxodG) relative to deoxyguanosine was measured following incubation of calf thymus DNA with KBrO(3) and GSH or N-acetylcysteine (NACys). This was dependent on these thiols and was associated with the loss of GSH and production of oxidized glutathione. A short-lived (<6 min) intermediate was apparent which did not react with the spin trap dimethylpyrroline N-oxide. DNA oxidation was not evident when potassium chlorate (KClO(3)) or potassium iodate (KIO(3)) were used instead of KBrO(3), though GSH depletion also occurred with KIO(3), but not with KClO(3). Other reductants and thiols in combination with KBrO(3) did not cause a significant increase in DNA oxidation. DNA strand breakage was also induced by KBrO(3) in human white blood cells (5 mM) and rat kidney epithelial cells (NRK-52E, 1.5 mM). This was associated with an apparent small depletion of thiols in NRK-52E cells at 15 min and with an elevation of 8-oxodG at a delayed time of 24 h. Depletion of intra-cellular GSH by diethylmaleate in human lymphocytes decreased the amount of strand breakage induced by KBrO(3). Extracellular GSH, however, protected against DNA strand breakage by KBrO(3), possibly due to the inability of the reactive product to enter the cell. In contrast, membrane-permeant NACys enhanced KBrO(3)-induced DNA strand breakage in these cells. DNA damage by KBrO(3) is therefore largely dependent on access to intracellular GSH.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2000

Nafenopin causes protein kinase C-mediated serine phosphorylation and loss of function of connexin 32 protein in rat hepatocytes without aberrant expression or localization.

The characteristics and mechanism of the inhibition of connexin-mediated gap junctional communication by the non-genotoxic rodent hepatocarcinogen, nafenopin, has been studied in rat hepatocytes. Nafenopin caused a time- and concentration-dependent inhibition of dye coupling in hepatocytes as assessed by transfer of microinjected lucifer yellow. A half-maximum inhibitory effect of nafenopin occurred at approximately 50 microM, which was not cytotoxic. The inhibitory effect was reversible since a significant recovery of communication was observed 3 h after removal of the chemical. The protein kinase inhibitor Gö6976 prevented the inhibition of dye coupling, but a tyrosine kinase inhibitor (genistein) did not. Connexin 32 and 26 protein expression, as assessed by immunoblotting, was similar in nafenopin-treated hepatocytes compared to controls, with the exception that in a 10-h culture with nafenopin, the level of connexin 26 was elevated compared to controls. Immunohistochemistry indicated that the localization of plaques containing connexin 32 was not affected in hepatocytes by nafenopin. Immunoprecipitated connexin 32 was, however, detected by an anti-phosphoserine antibody following nafenopin treatment, but not in controls. This serine phosphorylation was prevented in the presence of Gö6976. The results give further support for a role of protein kinase C in the post-translational inactivation of connexin 32 function in rat hepatocytes by nafenopin.

Animals↗