Lab report 3 Example | Topics and Well Written Essays - 3000 words

3 - Lab Report Example Studies have shown a generally low bioavailability and stability of oral catechins in humans. Nanoparticle-mediated delivery techniques of EGCG and TF have been found to improve their bioavailability to a level that would benefit their effectiveness as chemopreventives. The present study was conducted to compare the effects of theaflavins and EGCG, when used in the bulk form and in the biopolymer (polylactide-co-glycolide)-based nanoparticle form, on oxaliplatin- and satraplatin-treated lymphocytes from colorectal cancer patients and healthy volunteers. The results of DNA damage measurements by comet assay revealed opposite trends in bulk and nanoparticle forms of TF as well as EGCG. Both the compounds in the bulk form produced stastically significant concentration-dependent reductions in DNA damage in oxaliplatin- or satraplatin-treated lymphocytes. In contrast to this, when used in the nanoparticle form both TF and EGCG caused a concentration-dependent increase in DNA damage in the lymphocytes. The maximum increase noted with TF was around 2.5-fold. The reverse activities exhibited by the two forms, namely bulk- and nanoparticle forms, of TF as well as EGCG support the notion that TF and EGCG act as both antioxidant and pro-oxidant, depending on the form in which they are administered. In the bulk form, the compounds likely act as antioxidants, which was observed as a decrease in the DNA damage measured as Olive Tail Moment in the comet assays. It is also our hypothesis that, changing their mode of action in the nanoparticle form, both TF and EGCG act as pro-oxidants, and cause an increase in the DNA damage. Introduction One of the major causes of cancer development is oxidative stress. Oxidative stress leads to the cellular redox imbalance that has been observed in various cancer cells as compared to normal cells (Valko et al., 2006). Tissue homeostasis is disrupted when the balance between cell growth and apoptosis (cell death) is lost provoking uncontrolle d cell growth that results in cancer. Oxidative stress, which is prevalent in the tumour micro-environment, can affect the apoptotic potential of tumour cells. It can also affect many functions in cancer cells, including cell proliferation, promotion of mutations and genetic instability, modification of cellular sensitivity to anticancer compounds, invasion, and metastasis (Kumar et al., 2008). Reactive oxygen species (ROS) such as hydroxyl radicals, peroxides and superoxides, nitric oxide (NO') and peroxynitrite (ONOO-) that are generated in a normal cell both endogenously (by mitochondria, through metabolic processes, inflammation etc.) and via external sources, play a vital role in regulating several biological phenomena (Barzilai et al., 2002; Hussain et al, 2003). An excessive production of ROS or an inadequate anti-oxidant defense system, or both, in a normal cell can produce oxidative stress leading to DNA damage, and, further, induce an increased mutation rate and tumour dev elopment, possibly through a preferential selection of tumour cell mutations that confer a growth advantage (Sotgia et al., 2011). There is much evidence to show that oxidative stress plays an important role in the molecular mechanism of colorectal cancer (Keshavarzian et al., 1992; Bartsch et al., 2002). Free radicals formed during the metabolic activation of environmental genotoxic agents have been