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To determine the association of peroxisome proliferator activated receptor gamma coactivator 1 Gly482Ser variant with components of metabolic syndrome. A systematic search was carried out using Web of Science, PubMed, EMBASE and the Cochrane library using the key words: Peroxisome proliferator activator receptor gamma coactivator 1, PPARGC1A, PGC-1, PGC-1alpha, and PGC1alpha alone or with polymorphism, Gly482Ser and rs8192678. Data from 19 articles generated 28 separate data sets. Under the recessive model fasting plasma glucose was significantly lower in AA genotypes when compared to GG + GA in the total sample group and in non-Asian group (p <.001). The AA genotype showed significantly lower levels of total cholesterol compared to GG + GA genotype using the recessive model with the non-Asian group (p <.05). Under the dominant model, body mass index of the GG genotype was significantly higher in Asian subgroups (p <.05). PPARGC1A Gly482Ser variant impacts differently in Asian population groups. • This is the first meta-analysis where cholesterol has been used as an indicative element in the data search strategy for this variant; • The work demonstrates a genetic distinction at the level of the BMI between the Asian and non-Asian population groups; • AA genotype showed significantly lower levels of total cholesterol compared to GG + GA genotype in the non-Asian population. [ABSTRACT FROM AUTHOR]

Abstract: New naphthalimidopropyl, bisphthalimidopropyl and bisnaphthalimidopropyl (BNIP) derivatives were synthesised and characterised. Their interactions with Calf Thymus DNA were studied by UV spectrophotometric analysis and a competitive Ethidium bromide displacement assay. Cytotoxicity was determined by MTT assay in a breast cell system (MDA-MB-231 and MCF-10A cells). All BNIPs exhibited strong DNA-binding properties and cytotoxic activity with IC50 values in the range of 0.83–12.68 μM (24 and 48 h treatment). In addition, the uptake of BNIP derivatives within cancer cells was not via utilisation of the MGBG polyamine transporter. Put together the results confirm that the presence of the bisnaphthalimidopropyl and alkyl linker functionality are crucial for exerting DNA-binding and cytotoxic properties, hence demonstrating promise in their further development as potential anti cancer agents. [Copyright &y& Elsevier]

Abstract: Selenium (Se)-containing proteins have important roles in protecting cells from oxidative damage. This work investigated the effects of Se-depletion on the expression of the genes encoding selenoproteins in colonic mucosa from rats fed diets of different Se content and in human intestinal Caco-2 cells grown in Se-adequate or Se-depleted culture medium. Se-depletion produced statistically significant (P<0.05) falls in glutathione peroxidase (GPX) 1 mRNA (60–83%) and selenoprotein W mRNA (73%) levels, a small but significant fall in GPX4 mRNA (17–25%) but no significant change in GPX2. The data show that SelW expression in the colon is highly sensitive to Se-depletion. [Copyright &y& Elsevier]

To investigate the association between circulating levels of adipocytokines (adiponectin, leptin, tumour necrosis factor alpha (TNFα), interleukin 6 (IL-6)) and growth factors (insulin-like growth factor I (IGF-I) and II (IGF-II)), and the risk of endometrial cancer. Cochrane, CINAHL, Embase, Medline and Web of Science were searched for English-language manuscripts published between January 2000 and August 2018 using the following string of words: cancer and endometrial and (obesity or BMI) and (adiponectin or TNF* or IGF-I or IGF-II or IL-6 or leptin). Twenty articles were included in this meta-analysis, which corresponded to 18 studies involving 2921 endometrial carcinoma cases and 5302 controls. Fourteen articles reported circulating levels for adiponectin, seven for leptin, three for TNFα, three for IL-6 and one for IGF-I. No article reported values for IGF-II. Patients with circulating adiponectin levels in the highest tertile had decreased endometrial cancer risk compared to women with levels in the lowest tertile, (summary of odds ratio (SOR) 0.51, 95% confidence interval (CI): 0.38–0.69, p < 0.00001). Women with circulating leptin concentrations in the highest tertile had increased endometrial cancer risk compared to women with concentrations in the lowest tertile (SOR 2.19, 95% CI: 1.45–3.30, p = 0.0002). There was no difference in cancer risk between participants with the highest TNFα and IL-6 levels compared to the lowest levels (SOR 1.27, 95% CI: 0.88–1.83, p = 0.20 and SOR 1.20, 95% CI: 0.89–1.63, p = 0.23, respectively). Endometrial cancer risk is inversely affected by adiponectin and leptin levels. There appears to be no relationship between TNFα and IL-6 and the overall risk of endometrial cancer. • Patients with lower adiponectin levels are more likely to develop endometrial cancer despite BMI, hypertension or diabetes. • When considering BMI or a history of diabetes, increased leptin levels confer a greater risk of endometrial cancer. • Larger studies are required to establish the role of TNFα and IL-6 in the development of endometrial cancer. [ABSTRACT FROM AUTHOR]

Rapeseed pomace (RSP) is a waste product obtained after edible oil production from Brassica napus . Analysis of ubiquitous secondary metabolites in RSP samples (two breeds, harvested in 2012/2014 respectively from North East of Scotland) and their ethanol/water (95:5) Soxhlet extracts were carried out. Soxhlet extraction of the RSP (petroleum ether followed by 95% ethanol) gave a solid extract. LC-MS/MS data of the extracts revealed several secondary metabolites, with Sinapic acid being the most abundant. Strong antioxidant activities of the Soxhlet extracts were confirmed from the results obtained in the FRAP, DPPH and ORAC assays. Furthermore, for the very first time, RSP extracts (13.9 µg/ml) provided complete DNA protection, from oxidative stress induced by AAPH (3.5 mM). Therefore the strong antioxidant and DNA protecting properties demonstrated by the RSP extracts in this study warrants further investigation for their revalorisation and potential use as reliable source of antioxidants in different food applications. [ABSTRACT FROM AUTHOR]

Aim: The single-nucleotide polymorphism (SNP) rs713041, located in the regulatory region, is required to incorporate selenium into the selenoprotein glutathione peroxidase 4 (GPX4) and has been found to have functional consequences. This systematic review aimed to conduct a meta-analysis to determine whether there is an association between GPX4 (rs713041) SNP and the risk of diseases in humans and its correlation with selenium status. Material and methods: A systematic search for English-language manuscripts published between January 1990 and November 2022 was carried out using six databases: CINAHL, Cochrane, Medline, PubMed, Scopus and Web of Science. Odds ratios (ORs) and 95% confidence intervals (CIs) were applied to assess a relationship between GPX4 (rs713041) SNP and the risk of different diseases based on three genetic models. Review Manager 5.4 and Comprehensive Meta-Analysis 4 software were used to perform the meta-analysis and carry out Egger's test for publication bias. Results: Data from 21 articles were included in the systematic review. Diseases were clustered according to the physiological system affected to understand better the role of GPX4 (rs713041) SNP in developing different diseases. Carriers of the GPX4 (rs173041) T allele were associated with an increased risk of developing colorectal cancer in additive and dominant models (p = 0.02 and p = 0.004, respectively). In addition, carriers of the T allele were associated with an increased risk of developing stroke and hypertension in the additive, dominant and recessive models (p = 0.002, p = 0.004 and p = 0.01, respectively). On the other hand, the GPX4 (rs713041) T allele was associated with a decreased risk of developing pre-eclampsia in the additive, dominant and recessive models (p < 0.0001, p = 0.002 and p = 0.0005, respectively). Moreover, selenium levels presented lower mean values in cancer patients relative to control groups (SMD = −0.39 µg/L; 95% CI: −0.64, −0.14; p = 0.002, I2 = 85%). Conclusion: GPX4 (rs713041) T allele may influence colorectal cancer risk, stroke, hypertension and pre-eclampsia. In addition, low selenium levels may play a role in the increased risk of cancer. [ABSTRACT FROM AUTHOR]

Obesity is a major risk factor for several diseases, including metabolic syndrome (MetS), non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2D). The use of natural products, such as astaxanthin (ASX), a potent antioxidant compound produced by the freshwater green microalga Haematococcus pluvialis, has gained particular interest to reduce oxidative stress and inflammation, and to improve redox status, often associated with obesity. A systematic review and meta-analysis was performed to comprehensively examine the effects of ASX in animal models of diet induced obesity-associated diseases in order to inform the design of future human clinical studies for ASX use as supplement or nutraceutical. Cinahl, Cochraine, MEDLINE, Scopus and Web of Science were searched for English-language manuscripts published between January 2000 and April 2020 using the following key words: astaxanthin, obesity, non-alcoholic fatty liver disease, diabetes mellitus type 2, NAFLD and metabolic. Seventeen eligible articles, corresponding to 21 animal studies, were included in the final quantitative analysis. ASX, at different concentrations and administered for different length of time, induced a significant reduction in adipose tissue weight (P = 0.05) and systolic blood pressure (P < 0.0001) in control animals. In animal models of T2D, ASX significantly reduced serum glucose levels (P = 0.04); whereas it improved several disease biomarkers in the blood (e.g. cholesterol, triglycerides, ALT and AST, P < 0.10), and reduced liver (P = 0.0002) and body weight (P = 0.11), in animal models of NAFLD. Supplementation of ASX in the diet has positive effects on symptoms associated with obesity related diseases in animals, by having lipid-lowering, hypo-insulin and hypoglycaemic capacity, protecting organs from oxidative stress and mitigating the immune system, as suggested in this review. [Display omitted] • First meta-analysis on ASX effects in animal models of MetS, T2D and NAFLD. • ASX dietary supplementation positively affects symptoms in obesity related diseases. • ASX has lipid-lowering, hypo-insulin and hypoglycaemic capacity. • ASX protects organs from oxidative stress and modulates immune system. [ABSTRACT FROM AUTHOR]

Pancreatic cancer (PaCa) is one of the deadliest cancers known and its incidence is increasing in the developed countries. Because of the lack of biomarkers that allow early detection and the tendency of the disease to be asymptomatic, the diagnosis comes often too late for effective surgical or chemotherapy intervention. Lifestyle factors, that may cause common genetic modifications occurring in the disease, interfere with pancreatic physiology or function, and play a role in PaCa development, have been of concern recently, since a strategy to prevent this severe cancer is needed. This review identifies the latest evidences related to increased risk of developing PaCa due to dietary habits such as high alcohol, fructose and red or processed meat intake, and pathological conditions such as diabetes, obesity and infections in addition to stress and smoking behaviour. It aims to highlight the importance of intervening on modifiable risk factors: the action on these factors could prevent a considerable number of new cases of PaCa. • Smoking, high alcohol and red meat intake increase pancreatic cancer (PaCa) risk. • Obesity and diabetes stimulate insulin production and predispose to onset of PaCa. • Lifestyle and behaviour are linked with PaCa by plausible biological processes. • Inflammation a potential common mechanism to lifestyle environment, diseases and PaCa. [ABSTRACT FROM AUTHOR]

With increased longevity and subsequent rise in people with age‐related neurodegenerative diseases, protection of neurons from oxidative stress damage has become an important field of study. For the first time, we highlight the neuroprotective properties of rapeseed pomace (RSP) extract in SH‐SY5Y human neuroblastoma cells. We used resazurin to determine cell metabolism, 2,7'‐dichlorofluorescin diacetate (H2DCFDA) to assess the potential of RSP extracts to shield cells from reactive oxygen species (ROS) induced by H2O2 using flow cytometry, HPLC to analyze for malondialdehyde (MDA) as a lipid peroxidation marker and the COMET assay to assess DNA strand breakage. Protein stress arrays were used to investigate the cellular pathways affected by RSP extract. No effect on cell metabolism in SH‐SY5Y cells was observed after RSP extract treatment (up to 1.5 mg/ml). Pretreatment (24 hr) with RSP extract (1 mg/ml), before H2O2‐induced stress, alleviated ROS production and DNA strand breakage by 68%, and 38%, respectively. At protein level, the RSP extract increased the levels of FABP‐1, HIF‐1α, SOD2, and Cytochrome c proteins. Under H2O2‐induced stress, however, it helped to downregulate p38α levels, a protein kinase which is receptive to stress impulse (mitogen‐activated). RSP extract shows very promising cell protective properties in relation to oxidative stress. Practical applications: Oxidative stress has been associated with numerous diseases for example cancer, diabetes, and many neurological disorders including Parkinson's and Alzheimer's diseases. Hence, there is acceptance among the scientific community of antioxidant therapy and the quest for effective, low cost and readily available sources of natural antioxidants is paramount. Rapeseed plantations are abundant around the world due to the use of rapeseed oil in cooking and as a biofuel. The resulting rapeseed pomace (by‐product), specifically its extract, contains high levels of phytochemicals that protect cells against oxidative stress. Therefore, RSP extract can potentially be used/developed as functional food and nutraceuticals in the prevention of many complex neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Purpose: Maternal high-fat diet affects offspring and can induce metabolic disorders such as non-alcoholic fatty liver disease (NAFLD). New therapeutic strategies are being investigated as way to prevent or attenuate this condition. The objective of this study was to evaluate the effect of açaí supplementation in the maternal high-fat diet on dams and offspring lipid metabolism. Methods: Female Fisher rats were divided in four groups and fed a control diet (C), a high-fat diet (HF), an açaí supplemented diet (CA) and a high-fat diet supplemented with açaí (HFA) 2 weeks before mating, during gestation and lactation. The effects of açaí were evaluated in the male offspring after birth (P1) and weaning (P21). Results: HFA reduced relative liver weight, fat and cholesterol liver content in dams and improved liver steatosis as confirmed by histological analyses. HFA increased serum cholesterol and expression of Srebpf1 and Fasn genes. In offspring, HFA decreased relative liver weight, and serum cholesterol only in P21. An increase in the Sirt1, Srebpf1 and Fasn genes expression was observed in P21. Conclusions: These results suggest that açaí supplementation may attenuate NAFLD in dams and protect offspring from the detrimental effects of lipid excess from a maternal high-fat diet. [ABSTRACT FROM AUTHOR]

For a number of years there has been intense interest in phytochemicals due to their potential health benefits. One readily available and rich source of phytochemicals is Rapeseed pomace (RSP), a waste product obtained after edible oil production from Brassica napus . In this work, we analysed the ubiquitous secondary metabolites in RSP (harvest 2014, North East of Scotland) after soxhhlet ethanol/water (95:5) extraction. LC-MS/MS data of the extract revealed several secondary metabolites, with sinapic acid being the most abundant. The presence of a high level of phenolics in the extract was confirmed with the folin ciocalteu assay. Strong antioxidant activities of the extract was determined by using common antioxidant assays (FRAP, DPPH and ORAC). In addition, the extract (13.9 μg/mL) provided complete pBR322 plasmid DNA protection, from oxidative stress induced by AAPH (3.5 mM). Interestingly, in vitro analysis showed that the RSP extract exhibited acetylcholinesterase inhibition activity in a time and concentration dependant manner. Furthermore, cellular studies showed that incubation of neuroblastoma cells (SH Sy-5Y) with RSP extract protected cell metabolism from reactive oxygen species produced by H 2 O 2 (1 mM). We are currently undertaking in vivo studies using the model organism C. elegans . Preliminary results showed that RSP extract is non-toxic (up to 5 mg/mL) and has neuroprotective properties in C. elegans models of neurodegenerative diseases (work in progress). The positive properties associated with the RSP extract in this study warrants further investigation for the revalorisation of rapeseed pomace in the health/food industry. [ABSTRACT FROM AUTHOR]

Bisnaphthalimidopropyl diaminodicyclohexylmethane (BNIPDaCHM) bisintercalates to DNA and is a potential anti-cancer therapeutic. In an attempt to elucidate the mechanism(s) underlying the potential of BNIPDaCHM; earlier work was extended to investigate its effect on DNA damage and repair as well as cell cycle modulation, in a triple negative breast cancer (TNBC) cell line in vitro . BNIPDaCHM significantly decreased cell viability in a concentration (≥5 μM) and time (≥24 h) dependent manner. The mechanism of this growth inhibition involved alterations to cell cycle progression, an increase in the sub-G1 population and changes to plasma membrane integrity/permeability observed by flow cytometry and fluorescence microscopy with acridine orange/ethidium bromide staining. Using single cell gel electrophoresis (Comet assay) and fluorescence microscopy to detect γ-H2AX-foci expression; it was found that after 4 h, ≥ 0.1 μM BNIPDaCHM treatment-induced significant DNA double strand breaks (DSBs). Moreover, exposure to a non-genotoxic concentration of BNIPDaCHM induced a significant decrease in the repair of oxidative DNA strand breaks induced by hydrogen peroxide. Also, BNIPDaCHM-treatment induced a significant time dependent increase in p21 Waf/Cip1 mRNA expression but, did not alter p53 mRNA expression. In conclusion, BNIPDaCHM treatment in MDA-MB-231 cells was associated with a significant induction of DNA DSBs and inhibition of DNA repair at non-genotoxic concentrations via p53-independent expression of p21 Waf1/Cip1 . The latter may be a consequence of novel interactions between BNIPDaCHM and MDA-MB-231 cells which adds to the spectrum of therapeutically relevant activities that may be exploited in the future design and development of naphthalimide-based therapeutics. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MS) is a group of metabolic alterations that increase the susceptibility to cardiovascular disease and type 2 diabetes. Nonalcoholic fatty liver disease has been described as the liver manifestation of MS. We aimed to test the beneficial effects of an aerobic interval training (AIT) protocol on different biochemical, microscopic, and functional liver alterations related to the MS in the experimental model of obese Zucker rat. Two groups of lean and obese animals (6 weeks old) followed a protocol of AIT (4 min at 65%-80% of maximal oxygen uptake, followed by 3 min at 50%-65% of maximal oxygen uptake for 45-60 min, 5 days/week, 8 weeks of experimental period), whereas 2 control groups remained sedentary. Obese rats had higher food intake and body weight ( P < 0.0001) and suffered significant alterations in plasma lipid profile, area under the curve after oral glucose overload ( P < 0.0001), liver histology and functionality, and antioxidant status. The AIT protocol reduced the severity of alterations related to glucose and lipid metabolism and increased the liver protein expression of PPARγ, as well as the gene expression of glutathione peroxidase 4 ( P < 0.001). The training protocol also showed significant effects on the activity of hepatic antioxidant enzymes, although this action was greatly influenced by rat phenotype. The present data suggest that AIT protocol is a feasible strategy to improve some of the plasma and liver alterations featured by the MS. [ABSTRACT FROM AUTHOR]

Leptin is a hormone secreted by white fat tissue and signals the amount of overall body fat to the hypothalamus. The circulating concentration of leptin correlates with the level of obesity. Breast cancer risk is higher in obese postmenopausal women compared with postmenopausal women of a normal weight, and high leptin concentrations may contribute to this risk. In the present study, SK-BR-3 and MDA-MB-231 breast cancer cell lines were treated with various concentrations (6.25-1,600 ng?ml) of recombinant leptin and changes in cell proliferation were assessed. The SK-BR-3 breast cancer cells exhibited a concentration-dependent increase in proliferation with physiological leptin concentrations (<100 ng?ml), but no further increase in proliferation at high leptin concentrations (>100 ng?ml) was observed. Cell proliferation was not affected at supraphysiological leptin concentrations (>800 ng?ml) in SK-BR-3 cells, whereas it decreased in MDA-MB-231 cells. Therefore, cell signaling and cell cycle changes were assessed at supraphysiological concentrations (1,600 ng?ml). In the two cell lines, leptin treatment decreased the mitogen-activated protein kinase (MAPK) cell signaling pathway activation. Leptin treatment did not increase Akt phosphorylation or significantly alter the cell population distribution across cell cycle stages. To the best of our knowledge, leptin-induced growth inhibition of breast cancer cells at supraphysiological concentrations has not been reported in the literature to date, and the findings of this study suggest that reduced MAPK activity may be the underlying cause. Thus, the effect of leptin on breast cancer growth warrants further investigation since leptin is considered to be one of the main mediators in the obesity-breast cancer connection. [ABSTRACT FROM AUTHOR]

Lipids excess from an uterine environment can increase free radicals production of and thus induce oxidative status imbalance, a key factor for progression of non-alcoholic fatty liver disease (NAFLD) in offspring. Food antioxidant components in maternal diet may play an important role in preventing offspring metabolic disorders. The objective of the study was to evaluate the effects of açaí pulp supplementation on maternal high-fat diet, by assessing activity and expression of antioxidant enzymes and biomarkers of oxidative stress in the liver. Female Fisher rats were divided into four groups and fed a control diet (C), a high-fat diet (HF), a control diet supplemented with açaí (CA) and a high-fat diet supplemented with açaí (HFA) before mating, during gestation and lactation. The effects of açaí supplementation on oxidative stress biomarkers and antioxidant enzymes expression were evaluated in dams and male offspring after weaning. HFA diet increased body weight in dams, however reduced absolute and relative liver weight. There was a reduction in liver biomarkers of oxidative stress, malondialdehyde and carbonyl protein, as well as in catalase, glutathione peroxidase and superoxide dismutase activity. In offspring, HFA diet reduced liver weight and increased Gpx1, Gpx4 and Sod1 mRNA expression. These results suggest that açaí is able to restore redox status, preventing oxidative damage in dams by a direct mechanism and to promote beneficial effects on expression of antioxidant defences related genes in offspring. In this work, we demonstrated for the first time that açaí pulp supplementation to maternal high-fat diet may protect offspring from oxidative stress. These results showed a reduction in biomarkers of oxidative stress and antioxidants enzymes in dams. There was an increase in Gpx1, Gpx4 and Sod1 mRNA expression in offspring. Açaí pulp supplementation to maternal diet induced protection through modulation of oxidative stress by a direct mechanism in dams and may promote beneficial effects on antioxidant defences in offspring. [Display omitted] • Supplementation of açaí pulp to a maternal high fat diet prevents oxidative damage in dams and improves offspring antioxidant defences. • Supplementation of high fat diet with açaí reduces liver oxidative stress biomarkers. • Açaí supplementation to high fat diet reduces liver CAT, GPX, SOD activity in dams. • Açaí supplementation to maternal high fat diet reduces liver weight in offspring. • Maternal açaí supplemented high fat diet increases offspring liver Gpx1 , Gpx4, Sod1. [ABSTRACT FROM AUTHOR]

Periodic fasting (PF) is an increasingly popular approach that assists in the management of metabolic and inflammatory diseases as well as in preventing mechanisms involved in aging. However, little is known about the effects of fasting on gut microbiota and its impact on the epigenetic regulation of metabolically relevant enzymes, especially sirtuins (SIRTs). We analyzed the effect of periodic fasting on the human gut microbiota, SIRTs expression, and mitochondrial content in 51 males and females. The participants fasted under supervision for five consecutive days following the Buchinger fasting guidelines. Ketogenesis, selected mRNAs, miRNAs, mitochondrial (mt) DNA, and gut composition were analyzed before and after PF. PF triggered a significant switch in metabolism, as indicated by the increase in ß-hydroxybutyrate (BHB) and pyruvate dehydrogenase kinase isoform 4 (PDK4) expression in the capillary blood. MtDNA, SIRT1, SIRT3, and miRlet7b-5p expression in blood cells were elevated, whereas SIRT6 and miR125b-5p were not affected. Following fasting, gut microbiota diversity increased, and a statistically significant correlation between SIRT1 gene expression and the abundance of Prevotella and Lactobacillus was detected. The abundance of longevity related Christensenella species increased after fasting and inversely correlated with age as well as body mass index (BMI). Thus, this represents the first study that showing that fasting not only changes the composition of the gut microbiota, making it more diverse, but also affects SIRT expression in humans. [ABSTRACT FROM AUTHOR]

This special issue of Biochemical Pharmacology contains proceedings of a joint conference sponsored by the Natural Products Section of the International Union of Basic and Clinical Pharmacology (IUPHAR) and the International Conference on the Mechanism of Action of Nutraceuticals (ICMAN), an organization dedicated to defining actions and clinical benefits of pharmaceuticals and nutraceuticals. Entitled “From Nutraceuticals to Pharmaceuticals: Common Challenges and Approaches” , the conference was held in Aberdeen UK in September 2017. The aim of this gathering was to identify the challenges that must be overcome to identify and characterize novel therapeutics from natural products. Contained in this issue are reviews prepared by conference participants as well as abstracts describing oral and poster presentations. [ABSTRACT FROM AUTHOR]

Natural products have recently been exploited as alternative sources of cancer chemo-preventative agents. Induction of cell cycle arrest and apoptosis, and prevention of carcinogenesis and cancer progression are some of the mechanisms studied in cell systems and animal models. By-products from rapeseed oil extraction processes, however, have not been studied before: this study aims to assess the potential anti-cancer properties of extracts from rapeseed pomace (RSP), the by-product of cold pressed rapeseed oil production. RSP was extracted using accelerated solvent extraction (ASE) with different ethanol (EtOH) to water (dH 2 O) ratios: 50:50 EtOH:dH 2 O RSP extract showed significantly higher concentrations in Gallic Acid Equivalent (Folin Ciocalteu assay) compared to controls, and a significant increase in free radical scavenging properties (DPPH assay) was observed for 50:50 and 20:80 EtOH:dH 2 O RSP extracts. Moreover, extracts’ anticancer properties were assessed in a breast cancer cell line, MDA-MB-231. The three RSP extracts did not show cell cytotoxicity at concentrations ⩽1 mg/ml; however, at 2.5 mg/ml, 50:50 EtOH:dH 2 O RSP extract significantly decreased cell viability by 72% and, at 5 mg/ml, all extracts were cytotoxic. Cell treatment with 50:50 EtOH:dH 2 O RSP extract did not induce further DNA strand breaks (COMET assay) compared to untreated controls; however, an increase was measured with both 80:20 and 20:80 EtOH:dH 2 O RSP extracts. The anti-cancer properties of RSP extracts demonstrated in this study warrant further investigation and, potentially, open new avenues for the identification of chemo-preventative agents and reutilisation/revalorisation of rapeseed pomace. [ABSTRACT FROM AUTHOR]