Background: Hundreds of thousands around the world die from a disease caused by smoking cigarettes. Cigarette smoking (CS) is considered a worldwide major cause of preventable morbidity and mortality. The main clinical consequences of prolonged exposure to CS are chronic respiratory diseases, increased incidence of a variety of cancers, cigarette smoking had a dangerous effect on the essential biochemical mechanisms on the human body. Objective: This study aimed to assess the liver function in Sudanese male cigarettes smoker to identify the influence of cigarettes smoking on the level of their parameters. Material and methods: The study was designed as case control and include 81 samples, which is divided into case (51 samples) and control group (30 samples). The data collected by the use of questionnaire and blood specimens, and the levels of the parameters is measured by A15 automation spectrophotometer. Then the collected data is analyzed by the use of SPSS. Results: The results of the study showed statistically significant increase in total bilirubin and liver enzymes in case group when compared with control group. The mean of plasma total bilirubin, GOT (AST), GPT (ALT), and ALP levels in case group is (0.663, 26.49, 18.82 and 159.27) and in control group is (0.543, 23.00, 14.30 and 146.63) with p. value (0.001, 0.041, 0.004 and 0.000) respectively. And showed statistically insignificant decrease in total protein and albumin in case group when compared with control group, the means of total protein and albumin in case group is (66.47 and 33.73) and in control group is (68.30 and 34.43) with p. value (0.322 and 0.403) respectively. Conclusion: The study concluded that there was significant increase in liver enzymes (GOT, GPT, and ALP) and total bilirubin in cigarette smoking. And significant decrease in total protein and albumin, in cigarette smoking when compared to nonsmoking.

Colon cancer is a cancer begins in the large intestine (colon). Its aggression is due to late diagnosis, so poor prognosis and higher mortality rates are reported. Colon cancer has become a thorny research area that requires more examination of cellular pathways involved in its emergency. Based on this, we sought to check the biological role of cMyc in colon cancer cell proliferation through targeting its expression by a respective siRNA using CaCo-2 cell lines. Notably, the cytotoxic potential of cMyc knockdown was monitored by cell imaging using an inverted microscope, the production of lactate dehydrogenase (LDH) and viability of the transfected cells using MTT assay. The relative gene expression of c-myc and other related factors such as Raf-1 was investigated using quantitative real-time PCR (qRT-PCR). ELISA assay has been used to achieve the production of pro and anti-inflammatory cytokines released from transfected cells. Interestingly, the transfection with a new designed siRNA antagonist cMyc markedly decreased CaCo-2 cell viability rate in a dose-dependent manner compared with the transfection with specific siRNA antagonist Luciferase gene, which served as control. Likewise, number of survived cells significantly reduced following transfection with siRNA against c-myc, while the relative production of LDH significantly increased. Importantly, the cytotoxic effect of the transfection protocol showed neglected influence in normal colon epithelial cells (NCM-460 cell lines) indicating the selective regulation of colon cancer cell proliferation by transfection with siRNA targeting c-myc. Noteworthy, the knockdown efficiency of c-myc showed more than 80% inhibition of its expression in CaCo-2 cells transfected with the siRNA antagonist c-myc indicated by qRT-PCR. The relative gene expression of Raf-1 significantly decreased in c-myc knockdown cells, while the relative expression of both P53 and Caspase 3, as cell death indicators, significantly upregulated compared with control-transfected cells. Furthermore, the transfection with siRNA targeting c-myc markedly increased the production of interleukin 1 alpha (IL-1α ) and IL-1β, as pro-inflammatory cytokines, while decreased the production of IL- 4 and IL-10, as anti-inflammatory cytokines. These data provide evidence for the involvement of c-myc gene expression in colon cancer cell proliferation and immune response during cancer development.