Aims: Arsenic has carcinogenic properties because of the formation of Reactive Oxygen Species (ROS). ROS damages different macromolecules, tissues and organs, and severely exhausts cellular antioxidants.
Background: Cytosolic and mitochondrial contribution of ROS production by arsenic are not well reported. In regard to the issues of therapy against arsenic or any other toxicity, natural product has gained its popularity due to its less side-effects and non-invasive nature.
Objectives: Here, as an ethnomedicine, the flesh-extract (BBE; 100mg/100g bw) of Bellamya bengalensis (an aquatic mollusk) was applied in arsenic intoxicated (0.6 ppm/100g bw/for 28 days alone or in combination with BBE) experimental rats. Our objective was to study the anti-oxidative and anti-apoptotic role of BBE in hepato-gastrointestinal tissue damage by arsenic.
Methods: DNA fragmentation assay, catalase activity (gel-zymogram assay) suggests that BBE has a strong protective role against arsenic toxicity, which is decisively demonstrated in hepatic histoarchitecture study by HE (hematoxylin and eosin) staining and by intestinal PAS (Periodic Acid Schiff) staining.
Results: Measurement of mitochondrial-membrane-potential by fluorescent microcopy clearly demonstrated less membrane damage and lower release of the redox-active inner-membrane product (cytochrome-C, ubiquinone, etc.) in BBE supplemented group compared to that of the only arsenic fed group. The present study clearly suggests that mitochondrial disintegrity is one of the major causes of ROS mediated tissue damage by arsenic.
Conclusion: This study also offers an option for prevention/treatment against arsenic toxicity and its carcinogenicity by widely available low-cost, non-invasive Bellamya extract by protecting cytoskeleton, DNA and mitochondria in the cell.
[http://dx.doi.org/10.1016/j.jep.2011.09.009] [PMID: 21945824]
[http://dx.doi.org/10.1016/B978-0-12-416003-3.00001-9] [PMID: 22361177]
[http://dx.doi.org/10.1016/j.peptides.2011.01.014] [PMID: 21262297]
[http://dx.doi.org/10.1016/j.freeradbiomed.2013.03.022] [PMID: 23557727]
[http://dx.doi.org/10.1016/j.jep.2014.09.009] [PMID: 25291010]
[http://dx.doi.org/10.1034/j.1600-0676.2003.00837.x] [PMID: 12895266]
[http://dx.doi.org/10.1016/j.freeradbiomed.2009.09.013] [PMID: 19765645]