Antioxidant properties and stability of aegle marmelos leaves extracts

Aegle marmelos (AM) leaves were extracted with methanol (ME), ethanol (EE), water (WE) and analyzed for antioxidant activities by DPPH radical scavenging method, reducing power and in vitro inhibition by Fenton's reagent-induced oxidation of lipid system. Stability of extracts to pH (4, 7 and 9) and temperature (100 °C, 15 min.) was studied. The three extracts showed varying degree of efficacy in each assay in a dose dependent manner. The inhibition of MDA formation in Linseed oil by EE (47%) was significantly (P\textless0.05) higher than WE (28%) and ME (23%) but less than α- Tocopherol (80%). WE showed maximum stability to high temperature. The antioxidant activity of EE at pH 4 was significantly higher (P\textless0.05) compared with WE and ME. At pH 7, the antioxidant activity of all the three extracts remained unchanged. Data indicates that potential exists for the utilization of Aegle marmelos as a natural antioxidant. © 2011 Association of Food Scientists & Technologists (India)

Genotoxic and epigenetic mechanisms in arsenic carcinogenicity

Arsenic is a human carcinogen with weak mutagenic properties that induces tumors through mechanisms not yet completely understood. People worldwide are exposed to arsenic-contaminated drinking water, and epidemiological studies showed a high percentage of lung, bladder, liver, and kidney cancer in these populations. Several mechanisms by which arsenical compounds induce tumorigenesis were proposed including genotoxic damage and chromosomal abnormalities. Over the past decade, a growing body of evidence indicated that epigenetic modifications have a role in arsenic-inducing adverse effects on human health. The main epigenetic mechanisms are DNA methylation in gene promoter regions that regulate gene expression, histone tail modifications that regulate the accessibility of transcriptional machinery to genes, and microRNA activity (noncoding RNA able to modulate mRNA translation). The "double capacity" of arsenic to induce mutations and epimutations could be the main cause of arsenic-induced carcinogenesis. The aim of this review is to better clarify the mechanisms of the initiation and/or the promotion of arsenic-induced carcinogenesis in order to understand the best way to perform an early diagnosis and a prompt prevention that is the key point for protecting arsenic-exposed population. Studies on arsenic-exposed population should be designed in order to examine more comprehensively the presence and consequences of these genetic/epigenetic alterations. © 2014 Springer-Verlag