A huge volume of literature data suggests that a diet rich in fruits and vegetables, mostly due to the contribution of natural polyphenols, could reduce the incidence of specific cancers. Resveratrol, epigallocatechin gallate and curcumin are among the most extensively studied polyphenols: The majority of the effects attributed to these compounds are linked to their antioxidant and anti-inflammatory properties. The multiple mechanisms involved include the modulation of molecular events and signaling pathways associated with cell survival, proliferation, differentiation, migration, angiogenesis, hormonal activities, detoxification enzymes and immune responses. Notwithstanding their promising role in cancer prevention and treatment, polyphenols often have a poor bioavailability when administered as pure active principles, representing an important limit to their use. However, the bioavailability and thus the efficacy of these compounds can be improved by their administration in combination with other phytochemicals, with anticancer drugs or in polyphenol-loaded nanotechnology-based delivery systems. The possibility of combining conventional drugs with polyphenols offers very valuable advantages, such as the building of more efficient anticancer therapies with less side-effects on the health of patients. The present review focuses on current knowledge regarding the interactions between natural polyphenols and cancer development in order to gain a clearer comprehension of the potential mechanisms through which individual foods and food components may be exploited to reduce cancer risk. Contents 1. Introduction 2. Literature search 3. Classification of polyphenols 4. Prostate cancer 5. Colon cancer 6. Breast cancer 7. Lung cancer 8. Bladder cancer 9. Skin cancer 10. Pancreatic cancer 11. Leukemia 12. Conclusion

Environmental or occupational exposure to pesticides is considered one of the main risk factors for the development of various diseases. Behind the development of pesticide-associated pathologies, there are both genetic and epigenetic alterations, where these latter are mainly represented by the alteration in the expression levels of microRNAs and by the change in the methylation status of the DNA. At present, no studies have comprehensively evaluated the genetic and epigenetic alterations induced by pesticides; therefore, the aim of the present study was to identify modifications in gene miRNA expression and DNA methylation useful for the prediction of pesticide exposure. For this purpose, an integrated analysis of gene expression, microRNA expression, and DNA methylation datasets obtained from the GEO DataSets database was performed to identify putative genes, microRNAs, and DNA methylation hotspots associated with pesticide exposure and responsible for the development of different diseases. In addition, DIANA-miRPath, STRING, and GO Panther prediction tools were used to establish the functional role of the putative biomarkers identified. The results obtained demonstrated that pesticides can modulate the expression levels of different genes and induce different epigenetic alterations in the expression levels of miRNAs and in the modulation of DNA methylation status.

In recent years, new targets have been included between the health outcomes induced by pesticide exposure. The gastrointestinal tract is a key physical and biological barrier and it represents a primary site of exposure to toxic agents. Recently, the intestinal microbiota has emerged as a notable factor regulating pesticides’ toxicity. However, the specific mechanisms related to this interaction are not well known. In this review, we discuss the influence of pesticide exposure on the gut microbiota, discussing the factors influencing gut microbial diversity, and we summarize the updated literature. In conclusion, more studies are needed to clarify the host–microbial relationship concerning pesticide exposure and to define new prevention interventions, such as the identification of biomarkers of mucosal barrier function.

Abstract. Previous evidence has demonstrated that chemical classes of pesticides, including organophosphates (OP), can induce oxidative stress in exposed workers. The resulting increase in free radicals causes damage to biological macromolecules, and promotes the formation of novel compounds, including advanced glycation end products (AGE) and advanced oxidation protein products (AOPP). The present study aimed to evaluate the common genetic polymorphisms of the paraoxonase 1 (PON1) gene in a group of 55 farmers exposed to pesticides, as well as the association between these polymorphisms and serum levels of AGE and AOPP. The 192Q wild-type (WT) allele was present at a significantly higher frequency, compared with the 192R mutated allele (0.74 and 0.26, respectively). The WT allele was predominantly represented by the homozygote 192QQ genotype (51%). The mutated 192QR heterozygotic allele was prevalent, at a frequency of 45.4%, whereas the mutated homozygotes were present at a frequency of 3.6%. A significant decrease in the levels of AGE and AOPP was observed in farmers exhibiting the homozygotic 192RR mutated genotype (14,7221 AU/ml and 0.64 nmol/ml, respectively), compared with the WT genotype (16,1400 AU/ml and 1.76 nmol/ml, respectively), and 192QR genotype (15,2312 AU/ml and 1.60 nmol/ml, respectively). Therefore, due to the high catalytic activity of PON1, the 192RR genotype provides an important genetic predictor of the toxic effects associated with OP pesticide exposure. It determines a minor risk of developing oxidative damage following pesticide exposure, and measuring the levels of AOPP may provide a novel biomarker for oxidative damage in subjects exposed to OP.