Carcinogenicity In Experimental Animals Research Articles

Determination of Aflatoxins in Pig Feed. Using the Thin Layer Chromatography Technique

Aflatoxins are the most important mycotoxins in terms of food safety, due to their frequency and toxicity, they are characterized by being secondary metabolites synthesized by fungi. In order to determine the presence of aflatoxins in pork feed, five samples from different commercial companies were analyzed. The methodology used prior to the sample extraction process was the thin layer chromatography technique, observed using long-wave ultraviolet light. It could be seen in samples 1,3,4,5, the presence of Aflatoxins, toxicogenic strains of Aspergillus parasiticus, which produce aflatoxins, G1 and G2, is characterized by the fluorescence coloration, in sample 2 the presence was observed of aflatoxins toxicogenic strains of Aspergillus flavus. Toxigenic strains of Aspergillus flavus generally produce only aflatoxins B1 and B2, while toxicogenic strains of Aspergillus parasiticus produce aflatoxins B1, B2, G1 and G2. AFB1 aflatoxins have been considered obvious carcinogens in experimental animals. It is important to carry out systematic research with low-cost analytical techniques to understand the mechanisms of production and action of aflatoxins in foods, in order to prevent, monitor and control these types of toxins.

An Updated Review on the Psychoactive, Toxic and Anticancer Properties of Kava.

Kava (Piper methysticum) has been widely consumed for many years in the South Pacific Islands and displays psychoactive properties, especially soothing and calming effects. This plant has been used in Western countries as a natural anxiolytic in recent decades. Kava has also been used to treat symptoms associated with depression, menopause, insomnia, and convulsions, among others. Along with its putative beneficial health effects, kava has been associated with liver injury and other toxic effects, including skin toxicity in heavy consumers, possibly related to its metabolic profile or interference in the metabolism of other xenobiotics. Kava extracts and kavalactones generally displayed negative results in genetic toxicology assays although there is sufficient evidence for carcinogenicity in experimental animals, most likely through a non-genotoxic mode of action. Nevertheless, the chemotherapeutic/chemopreventive potential of kava against cancer has also been suggested. Both in vitro and in vivo studies have evaluated the effects of flavokavains, kavalactones and/or kava extracts in different cancer models, showing the induction of apoptosis, cell cycle arrest and other antiproliferative effects in several types of cancer, including breast, prostate, bladder, and lung. Overall, in this scoping review, several aspects of kava efficacy and safety are discussed and some pertinent issues related to kava consumption are identified.

Occupational exposure to antimony trioxide: a risk assessment

ObjectivesThe US National Toxicology Program (NTP) recently recommended in its Report on Carcinogens Monograph for Antimony Trioxide that antimony trioxide be listed as ‘reasonably anticipated to be a human carcinogen’...

The Association between Ranitidine Use and Gastrointestinal Cancers.

Simple SummaryN-nitrosodimethylamine (NDMA) is a carcinogen in experimental animals and has been classified a probable human carcinogen. NDMA has been identified in samples of ranitidine. Observational studies have demonstrated a relationship between dietary and occupational exposure to NDMA and specific cancers, principally to the gastrointestinal system. Studies focused on ranitidine exposure are lacking. This study evaluated the association between ranitidine exposure and gastrointestinal cancer using a comparison group that minimizes confounding by indication.N-nitrosodimethylamine (NDMA) is a carcinogen in experimental animals. It has been classified a probable human carcinogen and has been found in ranitidine. This study sought to evaluate the association between ranitidine use and cancer of the gastrointestinal system. Events reported to the FDA Adverse Events Reporting System that were associated with the use of proton pump inhibitors (PPIs) and H2 antagonists were selected. Proportionate reporting ratios (PRRs) and associated 95% confidence intervals (CIs) were calculated to compare the proportion of all reported adverse events that were for gastrointestinal system cancers among adverse event reports for ranitidine to adverse event reports for other H2 antagonists. The proportion of adverse events for any gastrointestinal system cancer relative to all other events was elevated for ranitidine compared to PPIs and other H2 antagonists (PRR 3.66, 95% CI 3.19–4.20). Elevated and significant PRRs were observed for pharyngeal (PRR 9.24), esophageal (PRR 3.56), stomach (PRR 1.48), colorectal (PRR 16.31), liver (PRR 2.64), and pancreatic (PRR 2.18) cancers. The PRRs for anal (PRR 4.62) and gallbladder (PRR 4.62) cancer were also elevated though not statistically significant. In conjunction with a large body of epidemiologic and human and animal basic science research, the study results support the hypothesis that NDMA-contaminated ranitidine increases the risk of cancer and supports the withdrawal of these medications from the market.

Maternal occupational benzo(a)pyrene exposure and risk of cancer in children

Background/Aim: The International Agency for Research on Cancer has classified benzo(a)pyrene (BaP) as carcinogenic to humans, based on sufficient evidence of carcinogenicity in experimental animals and supportive data on mechanistic pathways in humans. BaP is also a developmental toxicant. Yet, few studies assessed whether parental exposure to BaP is related to an increased risk for childhood cancers. Previous studies reported possible associations between environmental BaP exposure with risk increases in neuroblastoma and acute lymphoblastic leukemia. The aim of our study was to examine the relation between maternal occupational BaP exposure with risk of cancer in offspring.Methods: In this case-control study of Danish children (8339 cases, 208475 controls), we ascertained cases from the Cancer Registry and controls from the Central Population Register. Jobs during pregnancy were ascertained from the Supplemental Pension Fund, a mandatory supplement to the state pension. BaP exposure was determined via a job-exposure matrix developed for the Danish workforce. We used conditional logistic regression to determine associations with childhood cancer.Results: Ever occupational exposure to BaP during pregnancy was related to an increase in risk of neuroblastoma (Odds Ratio=1.65, 95% Confidence Interval 1.22, 2.23), while there was no increased risk for ALL (OR=1.02). We did not estimate any compelling risk increase for any other type of cancer, with effect estimates close to the null.Conclusions: This is the second study to report possible associations between BaP and neuroblastoma. Occupational exposures tend to be higher than ambient environmental exposures likely leading to greater fetal loss, which may in part explain variation in leukemia results compared to other studies.

Fumonisin B1 Epigenetically Regulates PTEN Expression and Modulates DNA Damage Checkpoint Regulation in HepG2 Liver Cells.

Fumonisin B1 (FB1), a Fusarium-produced mycotoxin, is found in various foods and feeds. It is a well-known liver carcinogen in experimental animals; however, its role in genotoxicity is controversial. The current study investigated FB1-triggered changes in the epigenetic regulation of PTEN and determined its effect on DNA damage checkpoint regulation in human liver hepatoma G2 (HepG2) cells. Following treatment with FB1 (IC50: 200 µM; 24 h), the expression of miR-30c, KDM5B, PTEN, H3K4me3, PI3K, AKT, p-ser473-AKT, CHK1, and p-ser280-CHK1 was measured using qPCR and/or Western blot. H3K4me3 enrichment at the PTEN promoter region was assayed via a ChIP assay and DNA damage was determined using an ELISA. FB1 induced oxidative DNA damage. Total KDM5B expression was reduced, which subsequently increased the total H3K4me3 and the enrichment of H3K4me3 at PTEN promoters. Increased H3K4me3 induced an increase in PTEN transcript levels. However, miR-30c inhibited PTEN translation. Thus, PI3K/AKT signaling was activated, inhibiting CHK1 activity via phosphorylation of its serine 280 residue preventing the repair of damaged DNA. In conclusion, FB1 epigenetically modulates the PTEN/PI3K/AKT signaling cascade, preventing DNA damage checkpoint regulation, and induces significant DNA damage.

Dietary Acrylamide Intake and the Risk of Liver Cancer: The Japan Public Health Center-Based Prospective Study.

Acrylamide has been studied for its carcinogenicity in experimental animals, causing tumors at several organ sites, and has been considered probably carcinogenic to humans as well. Given the small number of epidemiological studies that have been conducted, it is still uncertain whether the consumption of acrylamide is associated with liver cancer. Therefore, we investigated a study to determine the possible relationship between acrylamide intake and the risk of developing liver cancer in the Japanese population. A total of 85,305 participants, from the Japan Public Health Center-based Prospective Study, who provided a validated food-frequency questionnaire were enrolled between 1995 and 1998. During a median of 16.0 years follow-up, 744 new liver cancer cases were identified. Compared to the lowest tertile of acrylamide consumption (<4.8 µg/day), the multivariate hazard ratio (HR) for the highest tertile (≥7.6 µg/day) was 0.79 (95% confidence interval [CI] = 0.65–0.95) for liver cancer using multivariable model 1, adjusted for smoking status, body mass index (BMI), physical activity, medical history, and alcohol consumption; whereas the inverse relationship disappeared after additionally adjusting for coffee consumption in multivariable model 2 with HR of 1.08 (95% CI = 0.87–1.34) for the highest tertile. The effect of dietary acrylamide intake on the risk of liver cancer was not observed in the Japanese population.

Lack of potential carcinogenicity for aspartame – Systematic evaluation and integration of mechanistic data into the totality of the evidence

Despite repeated confirmation of aspartame safety in a variety of foods and beverages, there continues to be interest in researching the potential carcinogenic risk associated with its consumption. The objective of this evaluation was to conduct a systematic assessment of available mechanistic data using a framework for quantitatively integrating the key characteristics of carcinogens (KCCs). For aspartame, 1332 endpoints were appraised for quality and relevance and quantitatively integrated using an algorithm to determine the potential for individual KCC activity based on all available evidence, and subsequently assessed in the context of human and animal evidence streams. An overall lack of activity (integrated scores <0 and no “strong” categorizations) was observed for all KCCs except oxidative stressor (#5), for which activity was determined to be unlikely to be related to a carcinogenic response. Overall, the KCC-based analysis, together with the lack of consistent evidence of carcinogenicity in experimental animals, continue to support lack of carcinogenicity from aspartame consumption. This comprehensive evaluation of available mechanistic data demonstrates the need for a systematic approach to identify and appraise all avaialble data as part of weight-of-evidence determinations related use of KCC in evaluations of potential human carcinogenicity.

Chloroethene. Documentation of proposed values of occupational exposure limits (OELs)

Chloroethene. Documentation of proposed values of occupational exposure limits (OELs)

Carcinogenicity of multi-walled carbon nanotubes: challenging issue on hazard assessment.

Objectives: This report reviews the carcinogenicity of multi-walled carbon nanotubes (MWCNTs) in experimental animals, concentrating on MWNT-7, a straight fibrous MWCNT. Methods: MWCNTs were administered to mice and rats by intraperitoneal injection, intrascrotal injection, subcutaneous injection, intratracheal instillation and inhalation. Results: Intraperitoneal injection of MWNT-7 induced peritoneal mesothelioma in mice and rats. Intrascrotal injection induced peritoneal mesothelioma in rats. Intratracheal instillation of MWCNT-N (another straight fibrous MWCNT) induced both lung carcinoma and pleural mesothelioma in rats. In the whole body inhalation studies, in mice MWNT-7 promoted methylcholanthrene-initiated lung carcinogenesis. In rats, inhalation of MWNT-7 induced lung carcinoma and lung burdens of MWNT-7 increased with increasing concentration of airborne MWNT-7 and increasing duration of exposure. Conclusions: Straight, fibrous MWCNTs exerted carcinogenicity in experimental animals. Phagocytosis of MWCNT fibers by macrophages was very likely to be a principle factor in MWCNT lung carcinogenesis. Using no-observed-adverse-effect level-based approach, we calculated that the occupational exposure limit (OEL) of MWNT-7 for cancer protection is 0.15 μg/m3 for a human worker. Further studies on the effects of the shape and size of MWCNT fibers and mode of action on the carcinogenicity are required.

An overview of the toxicology and toxicokinetics of fusarenon-X, a type B trichothecene mycotoxin.

Fusarenon-X (FX) is a type B trichothecene mycotoxin that is frequently observed along with deoxynivalenol (DON) and nivalenol (NIV) in agricultural commodities. This review aims to give an overview of the literature concerning the toxicology and toxicokinetics of FX. FX is primarily found in cereals grown in temperate regions, but it can also be found worldwide because of the global transport of products. The major toxicity of FX occurs through inhibition of protein synthesis, followed by the disruption of DNA synthesis. Moreover, FX has also been shown to induce apoptosis in in vitro and in vivo studies. The targets of FX are organs containing actively proliferating cells, such as the thymus, spleen, skin, small intestine, testes and bone marrow. FX causes immunosuppression, intestinal malabsorption, developmental toxicity and genotoxicity. In addition, sufficient evidence of carcinogenicity in experimental animals is currently lacking, and the International Agency for Research on Cancer (IARC) classifies it as a group 3 carcinogen.

Extremely low-frequency magnetic fields and risk of childhood leukemia: A risk assessment by the ARIMMORA consortium.

Exposure to extremely low-frequency magnetic fields (ELF-MF) was evaluated in an International Agency for Research on Cancer (IARC) Monographs as "possibly carcinogenic to humans" in 2001, based on increased childhood leukemia risk observed in epidemiological studies. We conducted a hazard assessment using available scientific evidence published before March 2015, with inclusion of new research findings from the Advanced Research on Interaction Mechanisms of electroMagnetic exposures with Organisms for Risk Assessment (ARIMMORA) project. The IARC Monograph evaluation scheme was applied to hazard identification. In ARIMMORA for the first time, a transgenic mouse model was used to mimic the most common childhood leukemia: new pathogenic mechanisms were indicated, but more data are needed to draw definitive conclusions. Although experiments in different animal strains showed exposure-related decreases of CD8+ T-cells, a role in carcinogenesis must be further established. No direct damage of DNA by exposure was observed. Overall in the literature, there is limited evidence of carcinogenicity in humans and inadequate evidence of carcinogenicity in experimental animals, with only weak supporting evidence from mechanistic studies. New exposure data from ARIMMORA confirmed that if the association is nevertheless causal, up to 2% of childhood leukemias in Europe, as previously estimated, may be attributable to ELF-MF. In summary, ARIMMORA concludes that the relationship between ELF-MF and childhood leukemia remains consistent with possible carcinogenicity in humans. While this scientific uncertainty is dissatisfactory for science and public health, new mechanistic insight from ARIMMORA experiments points to future research that could provide a step-change in future assessments. Bioelectromagnetics. 37:183-189, 2016. © 2016 Wiley Periodicals, Inc.

Prevention of disease caused by fluoro-edenite fibrous amphibole: the way forward.

Few months after the publication of the monographic section of Annali dell'Istituto Superiore di Sanità second issue of 2014 "Health impact of fibres with fluoro-edenitic composition", the carcinogenicity of fluoro-edenite was assessed by the International Agency for Research on Cancer (IARC) in the frame of Monograph 111. The IARC Working Group concluded that there is sufficient evidence in humans that exposure to fluoro-edenite fibrous amphibole causes mesothelioma, and sufficient evidence of carcinogenicity in experimental animals. Fluoro-edenite was allocated to Group 1 (the agent is carcinogenic to humans). Now, in view of the recent IARC evaluation, preventive action in Biancavilla requires an upgrade. First of all, environmental monitoring has to be further implemented. All operations of house cleaning should be performed employing wet tools, in order to avoid dust-raising. It is very important that environmental and biological monitoring be related to epidemiological surveillance. The recently approved act of the Sicilian Government concerning a plan of health interventions in Biancavilla will favour cooperation between national, regional and local health institutions with the common goal of improving the quality and appropriateness of diagnostic and therapeutics procedures offered by the health services.

Dietary acrylamide intake and risk of endometrial cancer in prospective cohort studies.

Acrylamide has been associated with carcinogenicity in experimental animals, but potential health risks of dietary acrylamide intake and endometrial cancer in human are inconclusive. Thus, a meta-analysis of prospective cohort studies was conducted to provide a quantitative assessment of the association between dietary acrylamide intake and endometrial cancer risk. PubMed database was used to identify prospective cohort studies on dietary acrylamide intake and endometrial cancer risk published up to June 2014. Since smoking is an important source of acrylamide and is inversely associated with endometrial cancer risk, the association was examined in women who never smoked as well. Multivariable relative risks (RR) adjusting for potential confounders were combined using random effects models. Four large prospective cohort studies were identified, which included 453,355 female participants and 2,019 endometrial cancer cases. There was no association between dietary acrylamide intake and endometrial cancer risk overall [pooled RR for high vs. low intake = 1.10; 95% confidence interval (CI) 0.91-1.34]. High acrylamide intake, however, was significantly associated with increased risk of endometrial cancer among women who never smoked (pooled RR for high vs. low intake = 1.39; 95% CI 1.09-1.77). In dose-response analyses, pooled RRs for an increase of 10 µg/day were 1.04 (95% CI 0.97-1.11) among all women and 1.11 (95% CI 1.04-1.19) among never-smoking women. Endometrial cancer risk was not associated with dietary acrylamide intake overall. Among women who never smoked, however, there was a significantly increased endometrial cancer risk in women who consumed high dietary acrylamide.

Ethyl Carbamate in Fermented Beverages: Presence, Analytical Chemistry, Formation Mechanism, and Mitigation Proposals.

Ethyl carbamate (EC) commonly found in fermented beverages has been verified to be a multisite carcinogen in experimental animals. EC was upgraded to Group 2A by the Intl. Agency for Research on Cancer (IARC) in 2007, which indicates that EC is a probable carcinogen to humans. Because of its threat to human safety, the presence of EC may be a big challenge in the alcoholic beverage industry. During the past few years, thorough and systematic research has been carried out in terms of the generation of EC in order to meet the allowed limitation levels in fermented beverages. Previous studies have indicated that EC primarily results from the reaction of ethanol and compounds containing carbamyl groups. These main EC precursors are commonly generated from arginine metabolism by Saccharomyces cerevisiae or lactic acid bacteria accompanied by the fermentation process. This review comprehensively summarizes the genotoxicity, analytical methods, formation pathways, and removal strategies of EC in various beverages. The article also presents the metabolic mechanism of EC precursors and pertinent metabolites, such as urea, citrulline, and arginine.

The Weight of Evidence Does Not Support the Listing of Styrene as “Reasonably Anticipated to be a Human Carcinogen” in NTP's Twelfth Report on Carcinogens

ABSTRACT Styrene was listed as “reasonably anticipated to be a human carcinogen” in the twelfth edition of the National Toxicology Program's Report on Carcinogens based on what we contend are erroneous findings of limited evidence of carcinogenicity in humans, sufficient evidence of carcinogenicity in experimental animals, and supporting mechanistic data. The epidemiology studies show no consistent increased incidence of, or mortality from, any type of cancer. In animal studies, increased incidence rates of mostly benign tumors have been observed only in certain strains of one species (mice) and at one tissue site (lung). The lack of concordance of tumor incidence and tumor type among animals (even within the same species) and humans indicates that there has been no particular cancer consistently observed among all available studies. The only plausible mechanism for styrene-induced carcinogenesis—a non-genotoxic mode of action that is specific to the mouse lung—is not relevant to humans. As a whole, the evidence does not support the characterization of styrene as “reasonably anticipated to be a human carcinogen,” and styrene should not be listed in the Report on Carcinogens.

Metabolism, Genotoxicity, annd Carcinogenicity of Comfrey

Comfrey has been consumed by humans as a vegetable and a tea and used as an herbal medicine for more than 2000 years. Comfrey, however, produces hepatotoxicity in livestock and humans and carcinogenicity in experimental animals. Comfrey contains as many as 14 pyrrolizidine alkaloids (PA), including 7-acetylintermedine, 7-acetyllycopsamine, echimidine, intermedine, lasiocarpine, lycopsamine, myoscorpine, symlandine, symphytine, and symviridine. The mechanisms underlying comfrey-induced genotoxicity and carcinogenicity are still not fully understood. The available evidence suggests that the active metabolites of PA in comfrey interact with DNA in liver endothelial cells and hepatocytes, resulting in DNA damage, mutation induction, and cancer development. Genotoxicities attributed to comfrey and riddelliine (a representative genotoxic PA and a proven rodent mutagen and carcinogen) are discussed in this review. Both of these compounds induced similar profiles of 6,7-dihydro-7-hydroxy-1-hydroxymethyl-5H-pyrrolizine (DHP)-derived DNA adducts and similar mutation spectra. Further, the two agents share common mechanisms of drug metabolism and carcinogenesis. Overall, comfrey is mutagenic in liver, and PA contained in comfrey appear to be responsible for comfrey-induced toxicity and tumor induction.

Cancer risk assessment of ethyl carbamate in alcoholic beverages from Brazil with special consideration to the spirits cachaça and tiquira

BackgroundEthyl carbamate (EC) is a multi-site carcinogen in experimental animals and probably carcinogenic to humans (IARC group 2A). Traces of EC below health-relevant ranges naturally occur in several fermented foods and beverages, while higher concentrations above 1 mg/l are regularly detected in only certain spirits derived from cyanogenic plants. In Brazil this concerns the sugarcane spirit cachaça and the manioc (cassava) spirit tiquira, which both regularly exceed the national EC limit of 0.15 mg/l. This study aims to estimate human exposure in Brazil and provide a quantitative risk assessment.MethodsThe human dietary intake of EC via alcoholic beverages was estimated based on WHO alcohol consumption data in combination with own surveys and literature data. This data comprises the EC contents of the different beverage groups cachaça, tiquira, other spirits, beer, wine, and unrecorded alcohol (as defined by the WHO; including alcohol which is not captured in routine government statistics nor taxed). The risk assessment was conducted using the margin of exposure (MOE) approach with benchmark doses obtained from dose-response modelling of animal experiments. Lifetime cancer risk was calculated using the T25 dose descriptor.ResultsConsidering differences between pot-still and column-still cachaça, its average EC content would be 0.38 mg/l. Tiquira contained a considerably higher average EC content of 2.34 mg/l. The whole population exposure from all alcoholic beverages was calculated to be around 100 to 200 ng/kg bw/day, with cachaça and unrecorded alcohol as the major contributing factors. The MOE was calculated to range between 400 and 2,466, with the lifetime cancer risk at approximately 3 cases in 10,000. An even higher risk may exist for binge-drinkers of cachaça and tiquira with MOEs of up to 80 and 15, respectively.ConclusionsAccording to our risk assessment, EC poses a significant cancer risk for the alcohol-drinking population in Brazil, in addition to that of alcohol alone. Model calculations show that the implementation of the 0.15 mg/l limit for cachaça would be beneficial, including an increase of the MOE by a factor between 3 to 6. The implementation of policy measures for tiquira and unrecorded alcohol also appears to be advisable.

Abstract 869: The IARC Monographs Vol. 100. A critical review and update on human carcinogens

Abstract The IARC Monographs have been published continuously since 1971. For the 100th Vol. of the programme the evidence on all human carcinogens that have been identified to date has been updated. 147 experts from 28 countries contributed to the Vol. 100 series which was developed in six meetings from Oct 2008 to Oct 2009 (A. Pharmaceuticals, 23 agents; B. Biological agents, 11 agents; C. Metals, particles and fibres, 14 agents; D. Radiation, 14 agents; E. Lifestyle factors, 11 agents; F. Chemicals and related occupations, 34 agents). For each agent evaluations of the evidence in humans and in experimental animals and an overall evaluation of the human carcinogenicity have been developed and tumour sites with sufficient evidence of carcinogenicity as well as tumour sites that are strongly suspected and plausible mechanisms have been identified. All Group 1 carcinogens have been re-affirmed, several new Group 1 carcinogens and additional tumour sites for Group 1 carcinogens have been identified. Cancers of the colon, rectum and ovaries (mucinous type) have been added to the long list of tobacco smoking-related cancers, and parental smoking causes hepatoblastoma in the offspring and probably childhood leukemia. Acetaldehyde associated with alcohol consumption is carcinogenic to humans and causes cancers of the oesophagus, and head and neck. Based on sufficient evidence in humans for cutaneous and ocular melanoma, use of UV emitting tanning devices is now classified as “carcinogenic to humans”. In addition to lung cancer and mesothelioma, asbestos has now been linked with cancers of the larynx and ovaries, and leather dust has been identified as causing cancers of the nasal cavity and paranasal sinuses. There is now sufficient epidemiological evidence for TCDD exposure and all cancers combined, making TCDD the first agent classified initially in Group 1 based on sufficient animal data and mechanisms, to be later confirmed by increased cancer incidence in humans. Like TCDD, 2,3,4,7,8-pentachlordibenzofuran and 3,3’,4,4’, 5-pentachlorobiphenyl are complete carcinogens in experimental animals, and there is extensive evidence that they act through the same AhR-mediated mechanism. The Working Group classified these two chemicals in Group 1. The Working Group unanimously reaffirmed the classification of formaldehyde in Group 1, based on sufficient evidence in humans of nasopharyngeal cancer and concluded that, overall, there is sufficient evidence for leukaemia, particularly myeloid leukaemia. The re-affirmation of all group 1 carcinogens underlines the robust procedures and criteria for human carcinogen identification employed in the IARC Monographs Programme. Two additional Working Groups will be convened to develop scientific publications that build on the data that have been summarized in Volume 100: 1) Tumour-site concordance between humans and experimental animals; 2) Mechanisms involved in human carcinogenesis. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 869.

Comparative hepatotoxicity and clastogenicity of sodium arsenite and three petroleum products in experimental Swiss Albino Mice: The modulatory effects of Aloe vera gel

Petroleum products (PPs) consist of complex chemical mixtures, mainly hydrocarbons. Their composition varies considerably with source and use. Inappropriate manual handling and use of PPs, in countries like Nigeria, results in excessive skin contact with the possibility of hazard to health. There has been inadequate evidence to classify diesel, kerosene and hydraulic oil as human carcinogens and there is limited evidence for their toxicity and carcinogenicity in experimental animals. We compared the hepatotoxicity and clastogenicity of diesel, petrol or hydraulic oil with that of sodium arsenite (Na 2AsO 2) in mice. Our findings showed that these PPs are capable of inducing γ-glutamyl transferase (γGT) activity in the serum and liver to levels comparable with that induced by Na 2AsO 2. Mice treated with individual PPs have elevated mean liver and serum γGT at levels that are significantly different from the values observed for the negative control group. Also, the individual PPs alone have micronuclei formation induction activity similar to Na 2AsO 2. We found that treatment with Aloe vera gel before the PPs significantly reduced mean liver and serum γGT, and the mean number of micronuclei scored when compared with groups administered each of the PPs alone, supporting the presence of hepatoprotective components in Aloe vera.