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F Rojo

Publications and source records attributed to F Rojo.

At least 19 recordsLinked to original sources
PubMed2006

Phase I study of the humanised anti-EGFR monoclonal antibody matuzumab (EMD 72000) combined with gemcitabine in advanced pancreatic cancer.

The humanised anti-epidermal growth factor receptor (EGFR) monoclonal antibody matuzumab (formerly EMD 72000) is active against pancreatic cancer in preclinical studies. This phase I study assessed the safety and potential benefit of combined treatment with matuzumab and standard-dose gemcitabine. Three groups of chemotherapy-naive advanced pancreatic adenocarcinoma patients (n=17) received escalating doses of matuzumab (400 mg weekly, 800 mg biweekly, or 800 mg weekly) and gemcitabine (1000 mg m-2 weekly in weeks 1-3 of each 4-week cycle). Toxicity, antitumour activity, pharmacokinetic (PK) parameters, and pharmacodynamic (PD) markers in skin biopsies were evaluated. Severe treatment-related toxicities were limited to grade 3 neutropenia (n=3), leucopenia (n=1), and decreased white blood cell count (n=1). Common study drug-related adverse events were skin toxicities (grade 2=6, grade 1=7) and fever (grade 1=4). Matuzumab inhibited phosphorylated EGFR and affected receptor-dependent signalling and transduction; effects were seen even in the lowest-dose group. Pharmacokinetic data were consistent with results of matuzumab monotherapy. Partial response (PR) or stable disease occurred in eight of 12 evaluated patients (66.7%), with three PRs among six evaluated patients in the group receiving 800 mg weekly. Matuzumab in biologically effective doses with standard gemcitabine therapy appears well tolerated. The combination is feasible and may have enhanced activity.

Adenocarcinoma↗
PubMed2006

Study of microvessel density and the expression of the angiogenic factors VEGF, bFGF and the receptors Flt-1 and FLK-1 in benign, premalignant and malignant prostate tissues.

PURPOSE: Vascular endothelial growth factor (VEGF) is an angiogenic factor that stimulates endothelial cell growth and enhances vascular permeability. VEGF exerts its action by binding to the specific cell surface receptors, fms-like tyrosine kinase 1 (Flt-1) and fetal liver kinase 1 (FLK/KDR). In tumor angiogenesis, Vascular endothelial growth factor stimulates endothelial cells to produce Basic fibroblastic growth factor (bFGF), which further enhances angiogenic activity. Very little information on the expression of VEGF, bFGF, and the receptors Flt-1 and FLK/KDR is available. Herein, we evaluate the expression of these angiogenic factors and receptors in normal prostate, high grade prostate intraepithelial neoplasia (HGPIN) and prostatic cancer (CaP). MATERIALS AND METHODS: 58 selected surgical specimens exhibiting areas of normal prostate, HGPIN, and CaP were evaluated for microvessel density, and for VEGF, bFGF, Flt-1 and FLK/KDR protein expression by immunohistochemistry. Results were correlated with pathological data. RESULTS: There was a statistically significant increase in the microvessel density and in the expression of the angiogenic factors VEGF, bFGF and the receptors FLK/KDR and Flt-1, in the premalignant and malignant tissues in comparison with normal prostatic glands. Microvessel density also correlated with higher Gleason grade, pathological stage and the expression of the receptors FLK/KDR and Flt-1. CONCLUSIONS: The "initiation switch" of angiogenesis was observed to be an early event consistent with the recruitment of new vasculature into high grade PIN lesions and it increased in the progression of prostatic cancer.

Adenocarcinoma↗
PubMed2006

New p53 related genes in human tumors: significant downregulation in colon and lung carcinomas.

Human epithelial tumors need to accumulate multiple genetic alterations to form invasive carcinomas. These genetic alterations are related with growth factor receptors, cell signalling, the cell cycle and cell invasiveness. Importantly, cells need to avoid senescence and become immortalized for this process. Recently, five genes: RPS6KA6, HDAC4, KIAA0828, TCP1 and Tip60, which modulate p53-dependent function and avoid senescence were identified in a large-scale RNA interference screen. Twenty colon, 20 prostate and 20 lung carcinomas were studied to investigate whether these genes might be related with human tumors. RNA was extracted from both normal and tumor tissue from each patient. Real-time RT-PCR was performed using TaqMan probes corresponding to the RPS6KA6, HDAC4, KIAA0828, TCP1, Tip60 and p53 genes. In colon carcinomas, the RPS6KA6, HDAC4, KIAA0828 and Tip60 genes were downregulated in tumor tissue as compared with normal tissue (P < 0.001 for all genes). In lung carcinomas, HDAC4, KIAA0820 and Tip60 were downregulated (P < 0.01, P < 0.001 and P < 0.001 respectively). Whereas no significant differences were observed in prostate carcinomas, striking downregulation of the RPS6KA6 and KIAA0828 genes was observed in colon carcinomas and KIAA0828 in a subset of lung carcinomas. mRNA expression of these genes may control p53 function as well as the ras-MAPK pathway, methylation and transcriptional cellular programs. These results could unravel a novel set of regulatory suppressor genes involved in human colon and lung tumors.

Chaperonin Containing TCP-1↗
PubMed2004

Feasibility of CT scan-guided Tru-Cut serial liver biopsies to evaluate pharmacodynamic endpoints in patients with liver metastasis treated with experimental drugs.

We assessed the feasibility of using computed tomographically guided, Tru-Cut serial liver biopsies to perform pharmacodynamic studies in patients with liver metastasis who had been treated with experimental drugs. Twenty-three patients with liver metastasis were enrolled in two protocols for evaluation of the response to two new biologic drugs: a farnesyltransferase inhibitor and a tyrosine kinase inhibitor of the epidermal growth factor receptor. Computed tomographically guided Tru-Cut biopsies with an 18-gauge needle were performed. The procedure was performed at baseline and 2, 6, and 24 h after starting the administration of the drug. The procedures were scheduled on an outpatient basis. We obtained 271 samples (168 from metastatic lesions and 103 from surrounding normal liver tissue) from 23 patients. Biochemical determination of farnesyltransferase activity and different immunohistochemistry stainings (pEGRF, pMAPK, p27, Ki67, and apoptosis) of the signal transduction pathway were determined in each tissue sample, and all scheduled tissue assays were performed with the tissues obtained. Complete serial biopsies were performed in 20 patients. Three patients were excluded due to minor complications after the first biopsy. The morbidity rate in relation to the number of procedures was 1.1% (three of 271 samples). We found serial liver biopsies using Tru-Cut to be a safe and easy procedure. In our series, we could evaluate samples for molecular changes that influence the optimal dose, sequence, and schedule of the new antineoplastic agents.

Alkyl and Aryl Transferases↗
PubMed2004

Comparison of urinary sphingolipids in human populations with high and low maize consumption as a possible biomarker of fumonisin dietary exposure.

The increased sphinganine/sphingosine (SA/SO) ratio has previously been shown as a biomarker of fumonisin exposure in experimental animals and has been proposed as a tool to assess human exposure to fumonisin mainly occurring through the dietary consumption of fumonisin contaminated maize-based foods. Sphinganine and sphingosine were measured in urines of humans resident in two areas of North Argentina and South Brazil with high maize consumption and compared with urine samples collected in areas with very low or no maize consumption, such as Central Argentina and Southern Italy. The pattern of SA/SO values in the two groups with no maize consumption (assumed as controls) was similar, with all SA/SO values lower than one. Mean SA/SO ratio was 1.27 in urine of subjects with high maize consumption (n = 123) and 0.36 in controls (n = 66) and the difference was statistically significant (p<0.001). The mean fumonisin level in maize samples collected in North Argentina and South Brazil was 0.35 mg kg(-1) (n = 40). Although a similar maize and fumonisin intake was recorded for the two groups of populations, the mean SA/SO ratio in South Brazil (1.57) was significantly higher (p<0.05) than that of North Argentina (0.69). These data suggest that the higher SA/SO values observed in South Brazil cannot be associated with high fumonisin exposure and further studies are necessary to provide convincing evidence for using the SA/SO ratio as a biomarker of human fumonisin exposure.

Adolescent↗
PubMed2003

Aflatoxin B1 and its interconverting metabolite aflatoxicol in milk: the situation in Mexico.

Between 1996 and 1998, 580 litres of milk in Mexico were surveyed for aflatoxin B(1) (AFB(1)) and its metabolite aflatoxicol (AFL), which are mutagenic and carcinogenic mycotoxins that interconvert AFB(1)-AFL-AFB(1). The seven most consumed brands from different regions of Mexico included pasteurized and ultrapasteurized milk with four different fat levels: whole fat (28-33 g l(-1)), half-skimmed (10-20 g l(-1)), light (1-4 g l(-1)) and with vegetable oil (33 g l(-1)). Aflatoxins in each sample were concentrated with total aflatoxin immunoaffinity columns and quantitated by high-performance liquid chromatography. A milk sample was considered contaminated if it contained >/=0.05 microg l(-1) AFL. Pasteurization and ultrapasteurization of milk did not control contamination with AFL, which was present in 13% of samples at >/=0.05 microg l(-1) and in 8% at >/=0.5 microg l(-1), with a range of AFL from 0 to 12.4 microg l(-1). AFB(1) was present mainly in traces (0-0.4 microg l(-1)). The safest milk in relation to AFL contamination was imported milk powder with vegetable oil. There was a significant correlation between contamination of milk with AFL and the autumn (p<0.0002); the fat content was not significant.

Aflatoxin B1↗
PubMed2003

Increased tumour necrosis factor alpha production in mesenteric lymph nodes of cirrhotic patients with ascites.

BACKGROUND: Cytokines produced in mesenteric lymph nodes of cirrhotic rats with bacterial translocation may participate in circulatory alterations of cirrhosis. AIM: To investigate whether cirrhotic patients present an increased local generation of cytokines in mesenteric lymph nodes. METHODS: Mesenteric lymph nodes from 26 cirrhotic and 10 control patients were assessed for tumour necrosis factor alpha (TNF) and interleukin 6 mRNA and protein expression by competitive reverse transcription-polymerase chain reaction, and by enzyme immunoassay and immunohistochemistry, respectively. RESULTS: Interleukin 6 levels were not different between cirrhotics and controls. Protein and mRNA TNF levels in mesenteric lymph nodes from cirrhotics were higher than in controls (p<0.05). Tissue expression of TNF by immunohistochemistry was more abundant in cirrhotics. Ascitic patients showed higher TNF levels (47 (34-54) pg/mg protein) than patients without ascites (18 (17-25) pg/mg protein) (p<0.001). Elevated TNF levels (>28 pg/mg protein) in cirrhotics were associated with a higher Child-Pugh score, the antecedent of ascites, a lower prothrombin rate, and higher bilirubin and blood TNF levels. The strongest association, confirmed by multivariate analysis, was with the presence of ascites (p<0.001). Bacterial infections after transplantation, mainly by enteric bacteria, were only detected in patients with high TNF levels in mesenteric lymph nodes (33% of patients; p=0.05). CONCLUSION: Patients with advanced liver cirrhosis, and especially with ascites, have increased local production of TNF in mesenteric lymph nodes that, in common with experimental cirrhosis, may also be induced by bacterial translocation.

Ascites↗
PubMed2002

Phase I safety, pharmacokinetic, and pharmacodynamic trial of ZD1839, a selective oral epidermal growth factor receptor tyrosine kinase inhibitor, in patients with five selected solid tumor types.

PURPOSE: To establish the safety and tolerability of ZD1839 (Iressa), a selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, and to explore its pharmacokinetic and pharmacodynamic effects in patients with selected solid tumor types. PATIENTS AND METHODS: This was a phase I dose-escalating trial of oral ZD1839 150 mg/d to a maximum of 1,000 mg/d given once daily for at least 28 days. Patients with either advanced non-small-cell lung, ovarian, head and neck, prostate, or colorectal cancer were recruited. RESULTS: Eighty-eight patients received ZD1839 (150 to 1,000 mg/d). At 1,000 mg/d, five of 12 patients experienced dose-limiting toxicity (grade 3 diarrhea [four patients] and grade 3 somnolence [one patient]). The most frequent drug-related adverse events (AEs) were acne-like rash (64%) and diarrhea (47%), which were generally mild (grade 1/2) and reversible on cessation of treatment. No change in ZD1839 safety profile was observed with prolonged administration. Pharmacokinetic analysis showed steady-state exposure to ZD1839 in 98% of patients by day 7. Nineteen patients had stable disease and received ZD1839 for >or= 3 months; seven of these patients remained on study drug for >or= 6 months. Serial skin biopsies taken before treatment and at approximately day 28 revealed changes indicative of inhibition of the EGFR signaling pathway. CONCLUSION: ZD1839 was generally well tolerated, with manageable and reversible AEs at doses up to 600 mg/d and dose-limiting toxicity observed at 1,000 mg/d. ZD1839 treatment resulted in clinically meaningful disease stabilization across a range of tumor types and doses. Pharmacodynamic changes in skin confirmed inhibition of EGFR signaling, which was predicted from the mode of action of ZD1839.

Administration, Oral↗
PubMed2001

Activated extracellular signal-regulated kinases: association with epidermal growth factor receptor/transforming growth factor alpha expression in head and neck squamous carcinoma and inhibition by anti-epidermal growth factor receptor treatments.

The expression of the activated mitogen-activated kinases/extracellular signal-regulated kinases (ERKs) ERK1 and ERK2 was characterized in 101 humanhead and neck squamous carcinoma specimens. Activated ERK1/2were detected at different levels in the majority of these tumors, as assayed by immunostaining with an antibody specific for the dually phosphorylated and activated ERK1 and ERK2. ERK1/2 activation levels were higher in tumors with advanced regional lymph node metastasis (P = 0.048) and in relapsed tumors (P = 0.021). The expression of epidermal growth factor (EGF) receptor (P = 0.037), transforming growth factor alpha (TGF-alpha; P < 0.001), and HER2 (P = 0.066; positive trend) correlated with activation of ERK1/2. In a multivariate analysis, both TGF-alpha (P < 0.0001) and HER2 (P = 0.045) were independently correlated with ERK1/2 activation. In turn, activation of ERK1/2 was associated with a higher Ki-67 proliferative index (P = 0.002). In EGF receptor-dependent model cells (A431 and DiFi), a specific EGF receptor tyrosine kinase inhibitor ("Iressa"; ZD1839) and a chimeric anti-EGF receptor antibody ("Cetuximab"; C225) inhibited ERK 1/2 activation at concentrations that inhibited autocrine cell proliferation. In patients on treatment with C225, the activation of ERK1/2 in skin, an EGF receptor-dependent tissue, was lower compared with control skin. Parallel changes were seen in keratinocyte Ki67 proliferation indexes in skin from C225-treated patients. Taken together, these studies provide support for a role of activation of ERK1/2 in head and neck squamous carcinoma and a correlation with EGF receptor/TGF-alpha expression. The inhibition of ERK1/2 activation in vitro and in vivo by compounds targeting the EGF receptor points to the interest of ERK1/2 as potential surrogate markers of EGF-receptor signaling in clinical therapeutic studies.

Adult↗
PubMed2001

Trastuzumab (herceptin), a humanized anti-Her2 receptor monoclonal antibody, inhibits basal and activated Her2 ectodomain cleavage in breast cancer cells.

HER2 is a ligand-less tyrosine kinase receptor of the ErbB family that is frequently overexpressed in breast cancer. It undergoes proteolytic cleavage that results in the release of the extracellular domain and the production of a truncated membrane-bound fragment, p95. We show that HER2 shedding is activated by 4-aminophenylmercuric acetate (APMA), a well-known matrix metalloprotease activator, in HER2-overexpressing breast cancer cells. The HER2 p95 fragment, which appears after APMA-induced cleavage, is phosphorylated. We analyzed 24 human breast cancer specimens, and a phosphorylated M(r) 95,000 HER2 band could be detected in some of them, which indicated that the truncated receptor is also present in vivo. The activation of HER2 shedding by APMA in cells was blocked with batimastat, a broad-spectrum metalloprotease inhibitor. Trastuzumab (Herceptin; Genentech, San Francisco, CA), a humanized monoclonal antibody directed at the HER2 ectodomain, which has been shown to be active in patients with HER2-overexpressing breast cancer, inhibited basal and induced HER2 cleavage and, as a consequence, the generation of phosphorylated p95. This inhibitory effect of trastuzumab was not shared by 2C4, an antibody against a different epitope of the HER2 ectodomain. The inhibition of basal and APMA-induced cleavage of HER2 by trastuzumab preceded antibody-induced receptor down-modulation, which indicated that the effect of trastuzumab on cleavage was not attributable to a decrease in cell-surface HER2 induced by trastuzumab. We propose that the inhibition of HER2 cleavage and prevention of the production of an active truncated HER2 fragment represent a novel mechanism of action of trastuzumab.

Adenocarcinoma↗
PubMed2001

A Mutation in the C-terminal domain of the RNA polymerase alpha subunit that destabilizes the open complexes formed at the phage phi 29 late A3 promoter.

Regulatory protein p4 from Bacillus subtilis phage phi29 activates the viral late A3 promoter mainly by stabilizing the binding of RNA polymerase (RNAP) to it as a closed complex. This requires an interaction between protein p4 residue Arg120 and the C-terminal domain (CTD) of the RNAP alpha subunit. Several acidic residues of the alpha-CTD, considered as plausible targets for p4 residue Arg120, were individually changed into alanine. In addition, a truncated alpha subunit lacking the last four residues, two of which are acidic, was obtained. The modified alpha subunits were purified and reconstituted into RNAP holoenzyme in vitro. Protein p4 was found to be unable to activate the late A3 promoter when residue Glu297 of the alpha subunit was changed to Ala, a modification that did not impair transcription from several other promoters. Interestingly, protein p4 could stabilize the modified RNAP at the A3 promoter as a closed complex, although the open complexes formed were unstable and did not proceed to elongation complexes. Our results indicate that the change of the alpha residue Glu297 into Ala destabilizes the open complexes formed at this promoter, but not at other promoters. Considered in the context of earlier findings indicating that the RNAP alpha-CTD may participate in the transition from closed to intermediate complexes at some other promoters, the new results expand and clarify our view of its role in transcription initiation.

Amino Acid Sequence↗
PubMed2001

Pharmacodynamic studies with the epidermal growth factor receptor tyrosine kinase inhibitor ZD1839.

ZD1839 is an orally active, selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that blocks signal transduction pathways implicated in the proliferation and survival of cancer cells, and other host-dependent processes promoting cancer growth. Based on its promising preclinical antitumor activity and favorable toxicity profile, ZD1839 has recently entered clinical trials. A particular challenge in the clinical development of this exciting compound is to explore its biological (pharmacodynamic) activity against the EGFR and receptor-dependent processes in serial biopsies. Such studies might be of assistance in predicting the subset of tumors that will benefit from therapy. They also may prove whether complete EGFR blockade is achieved in vivo. This latest point is particularly relevant because an optimal biological dose (ie, a dose resulting in complete receptor inhibition) would be preferred to the maximally tolerated dose that is being used with conventional nontargeted chemotherapeutic drugs. A series of preclinical studies have identified potentially useful surrogate markers of EGFR activity (eg, phosphorylation of EGFR and downstream receptor-dependent molecules such as mitogen-activated protein kinase [MAPK], Akt, or p27) that could be used as a surrogate marker of ZD1839 efficacy. In various tumor types, such as head and neck squamous carcinoma and gastric and breast adenocarcinoma, a relationship between EGFR and downstream markers (such as phosphorylated MAPK) has been characterized, further supporting the potential of these molecules for pharmacodynamic studies. Preliminary analysis of serial skin biopsies from patients participating in phase I trials has shown that ZD1839 results in substantial changes in EGFR-dependent molecules, such as phosphorylated MAPK, p27, phosphorylated STAT3, and others. Based on these encouraging results, studies assessing activated EGFR, activated MAPK, and other selected markers in phase II trials in tumors from patients treated with ZD1839 are currently planned or ongoing.

Animals↗
PubMed2001

Mechanisms of transcriptional repression.

Transcriptional repressors are usually viewed as proteins that bind to promoters in a way that impedes subsequent binding of RNA polymerase. Although this repression mechanism is found at several promoters, there is a growing list of repressors that inhibit transcription initiation in other ways. For example, several repressors allow the simultaneous binding of RNA polymerase to the promoter, but interfere with subsequent events of the initiation process, eventually inhibiting transcription initiation. The recent increase in the number of repressors for which the repression mechanism has been characterized in detail has shown an amazing variety of strategies to repress transcription initiation. It is not surprising to find that the repression mechanism used is usually exquisitely adapted to the characteristics of the promoter and of the repressor involved.

Archaeal Proteins↗
PubMed2001

The alkane hydroxylase gene of Burkholderia cepacia RR10 is under catabolite repression control.

In many microorganisms the first step for alkane degradation is the terminal oxidation of the molecule by an alkane hydroxylase. We report the characterization of a gene coding for an alkane hydroxylase in a Burkholderia cepacia strain isolated from an oil-contaminated site. The protein encoded showed similarity to other known or predicted bacterial alkane hydroxylases, although it clustered on a separate branch together with the predicted alkane hydroxylase of a Mycobacterium tuberculosis strain. Introduction of the cloned B. cepacia gene into an alkane hydroxylase knockout mutant of Pseudomonas fluorescens CHAO restored its ability to grow on alkanes, which confirms that the gene analyzed encodes a functional alkane hydroxylase. The gene, which was named alkB, is not linked to other genes of the alkane oxidation pathway. Its promoter was identified, and its expression was analyzed under different growth conditions. Transcription was induced by alkanes of chain lengths containing 12 to at least 30 carbon atoms as well as by alkanols. Although the gene was efficiently expressed during exponential growth, transcription increased about fivefold when cells approached stationary phase, a characteristic not shared by the few alkane degraders whose regulation has been studied. Expression of the alkB gene was under carbon catabolite repression when cells were cultured in the presence of several organic acids and sugars or in a complex (rich) medium. The catabolic repression process showed several characteristics that are clearly different from what has been observed in other alkane degradation pathways.

Alkanes↗
PubMed2001

Role of the crc gene in catabolic repression of the Pseudomonas putida GPo1 alkane degradation pathway.

Expression of the alkane degradation pathway encoded in the OCT plasmid of Pseudomonas putida GPo1 is induced in the presence of alkanes by the AlkS regulator, and it is down-regulated by catabolic repression. The catabolic repression effect reduces the expression of the two AlkS-activated promoters of the pathway, named PalkB and PalkS2. The P. putida Crc protein participates in catabolic repression of some metabolic pathways for sugars and nitrogenated compounds. Here, we show that Crc has an important role in the catabolic repression exerted on the P. putida GPo1 alkane degradation pathway when cells grow exponentially in a rich medium. Interestingly, Crc plays little or no role on the catabolic repression exerted by some organic acids in a defined medium, which shows that these two types of catabolic repression can be genetically distinguished. Disruption of the crc gene led to a six- to sevenfold increase in the levels of the mRNAs arising from the AlkS-activated PalkB and PalkS2 promoters in cells growing exponentially in rich medium. This was not due to an increase in the half-lives of these mRNAs. Since AlkS activates the expression of its own gene and seems to be present in limiting amounts, the higher mRNA levels observed in the absence of Crc could arise from an increase in either transcription initiation or in the translation efficiency of the alkS mRNA. Both alternatives would lead to increased AlkS levels and hence to elevated expression of PalkB and PalkS2. High expression of alkS from a heterologous promoter eliminated catabolic repression. Our results indicate that catabolic repression in rich medium is directed to down-regulate the levels of the AlkS activator. Crc would thus modulate, directly or indirectly, the levels of AlkS.

Alkanes↗
PubMed2001

Analysis of early promoters of the Bacillus bacteriophage GA-1.

Bacteriophage GA-1, which infects Bacillus sp. strain G1R, is evolutionarily related to phage phi29, which infects Bacillus subtilis. We report the characterization of several GA-1 promoters located at either end of its linear genome. Some of them are unique for GA-1 and drive the expression of open reading frames that have no counterparts in the genome of phi29 or related phages. These unique promoters are active at early infection times and are repressed at late times. In vitro transcription reactions revealed that the purified GA-1-encoded protein p6 represses the activity of these promoters, although the amount of p6 required to repress transcription was different for each promoter. The level of protein p6 produced in vivo increases rapidly during the first stage of the infection cycle. The protein p6 concentration may serve to modulate the expression of these early promoters as infection proceeds.

Bacillus Phages↗
PubMed2000

Characterization of bacterial strains able to grow on high molecular mass residues from crude oil processing.

Oil residues containing high molecular mass hydrocarbons, rich in polyaromatic compounds, are frequent end-products of crude oil processing and are poorly biodegradable. Their disposal poses an environmental problem. Through batch-enrichments from contaminated soils we have isolated and characterized seven bacterial strains that can use a residue from crude oil processing as a source of carbon and energy. The residue was a complex mixture of high molecular mass compounds, including saturated, aromatic and polycyclic aromatic hydrocarbons (PAHs). Analysis of the metabolic profiles of the strains isolated showed that they could all metabolize long-chain-length alkanes efficiently, but not PAHs. Strains degrading naphthalene, a simple PAH, did exist in the soil inocula used, but could be isolated only when enrichments were performed using pure naphthalene as the sole carbon source. All strains tested emulsified the oil residue and their ability to produce surfactants was studied.

Journal Article↗