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

3 - Lab Report ExampleStudies have shown a generally small(a) 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 put on their effectiveness as chemopreventives. The present study was conducted to compare the effects of theaflavins and EGCG, when used in the bulk radiation pattern and in the biopolymer (polylactide-co-glycolide)-based nanoparticle melodic phrase, on oxaliplatin- and satraplatin-treated lymphocytes from colorectal cancer patients and healthy volunteers. The results of DNA damage measurements by comet assay revealed foe trends in bulk and nanoparticle forms of TF as well as EGCG. Both the compounds in the bulk form produced stastically prodigious 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 conc entration-dependent increase in DNA damage in the lymphocytes. The maximum increase famed 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 supposition 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 credibly act as antioxidants, which was observe as a decrease in the DNA damage mensurable as Olive Tail Moment in the comet assays. It is also our hypothesis that, changing their mode of perform in the nanoparticle form, both TF and EGCG act as pro-oxidants, and cause an increase in the DNA damage. Introduction mavin of the major causes of cancer development is oxidative stress. Oxidative stress leads to the electric cellphoneular 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 bal ance between cell growth and apoptosis (cell death) is lost provoking uncontrolled cell growth that results in cancer. Oxidative stress, which is plethoric in the neoplasm micro-environment, can affect the apoptotic potential of tumour cells. It can also affect numerous 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). labile 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, establish an increased mutation rate and tumour development, 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 form during the metabolic activation of environmental genotoxic agents have been