Effect of Smoke Exposure on Chronic Inflammation and P53 Expression in Pelvis Epithelial

Many risk factors can cause upper urinary tract carcinoma. Smoking is the most influential risk factor and is associated with the formation of aromatic acids and could induce apoptotic cycle. This research was aimed to examine the effect of cigarete smoke exposure on inflammatory state and p53 expression in renal pelvis epithelial of wistar rats. As many as 25 male rats aged 6-8 weeks were divided into five groups as follows: Control (without treatment); CS-1, CS-2, CS-4, and CS-8 (treated with CS 1x, 2x, 4x, and 8x/day, respectively). Each exposure was done for 15 minutes for 60 days. histopathological changes were evaluated from HE-stained specimens and immunohistochemistry method was applied to measure p53 expressio neutrophile and lymphocyte count in CS-8 was significantly higher as compared to CS-1 (p<0.05) and control (p<0.05). p53 expression was found in the CS-8 (3 out of 5 subjects had positive p53 expression, with a total of 4-7 cells from 10 hpf). Correlation study showed significant correlation between frequency of cigarette smoking exposure and neutrophile count (p=0.000; r=-0.856); lymphocyte count (p=0.000; r=0.985); and p53 expression (p=0.000; 0.072). We concluded that there were significant differences in acute inflammation state, chronic inflammation state and p53 expression among groups. Correlation study showed that frequency of cigarette smoking exposure was positively correlated with lymphocyte count and p53 expression.

Download Full-text

Effect of Smoke Exposure on Chronic Inflammation and P53 Expression in Bladder Epithelial

International Journal of Innovative Technology and Exploring Engineering - Special Issue ◽

10.35940/ijitee.c1069.0193s20 ◽

2020 ◽

Vol 9 (3S) ◽

pp. 41-46

Keyword(s):

Cigarette Smoking ◽

Chronic Inflammation ◽

Wistar Rats ◽

Correlation Study ◽

Monocyte Count ◽

P53 Expression ◽

Inflammatory Score ◽

Smoking Exposure ◽

Inflammatory State ◽

Cigarette Smoking Exposure

Bladder cancer is widely studied for its association with cigarette smoke (CS) exposure. Nicotine and carcinogenic substances in CS could induce chronic inflammatory state and DNA damage. This research was aimed to investigate the effect of CS exposure in chronic inflammatory state and p53 expression in bladder epithelial of Wistar rats. 25 male Wistar rats aged 6-8 weeks were divided into five groups as follows: Control (without treatment); CS-1, CS-2, CS-4, and CS-8 (treated with CS 1x, 2x, 4x, and 8x/day, respectively). Each exposure was done for 15 minutes for 60 days. Chronic inflammatory score was calculated from HE-stained specimens and Immunohistochemistry method was applied to measure p53 expression. Results showed that lymphocyte and histiocyte count in CS-8 was significantly higher as compared to CS-1 (p<0.05) and control (p<0.05). Lymphocyte and histiocyte count in CS-4 was also significantly higher compared to non-treated group (p<0.05). Chronic inflammatory score was significantly higher in CS-8 compared to other group (p<0.05). Moreover, p53 expression was found in CS-8 group (2 of 5 subjects had positive p53 expression, 20 positive cells in from total 10 hpf) and significantly different with other groups (p=0.011). Correlation study showed significant correlation between frequency of cigarette smoking exposure and lymphocyte count (p=0.000; r=0.956); monocyte count (p=0.000; r=0.928); chronic inflammation score (p=0.000; r=0.928); and p53 expression (p=0.007; r=0.522). We concluded that there was significant differences in chronic inflammation state and p53 expression among groups. Correlation study showed that frequency of cigarette smoking exposure was positively correlated with chronic inflammation and p53 expression.

Download Full-text

Concentrations of Blood Vitamin A, C, E, Coenzyme Q10 and Urine Cotinine Related to Cigarette Smoking Exposure

Annals of Laboratory Medicine ◽

10.3343/kjlm.2009.29.1.10 ◽

2009 ◽

Vol 29 (1) ◽

pp. 10-16 ◽

Cited By ~ 5

Author(s):

Sean-Mi Song ◽

Yong-Sun Park ◽

Anna Lee ◽

Yong Gon Cho ◽

Dal Sik Kim ◽

...

Keyword(s):

Cigarette Smoking ◽

Vitamin A ◽

Coenzyme Q10 ◽

Urine Cotinine ◽

Smoking Exposure ◽

Cigarette Smoking Exposure

Download Full-text

Airway inflammation and remodeling of cigarette smoking exposure ovalbumin-induced asthma is alleviated by CpG oligodeoxynucleotides via affecting dendritic cell-mediated Th17 polarization

International Immunopharmacology ◽

10.1016/j.intimp.2020.106361 ◽

2020 ◽

Vol 82 ◽

pp. 106361

Author(s):

Hong-tao Li ◽

Yu-sen Lin ◽

Qi-mei Ye ◽

Xue-na Yang ◽

Xiao-ling Zou ◽

...

Keyword(s):

Dendritic Cell ◽

Cigarette Smoking ◽

Airway Inflammation ◽

Cpg Oligodeoxynucleotides ◽

Smoking Exposure ◽

Cigarette Smoking Exposure

Download Full-text

P6136Intense daily cigarette smoking accelerates vascular damage of smokers with a moderate cumulative tobacco smoke exposure

European Heart Journal ◽

10.1093/eurheartj/ehz746.0743 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

N Ioakeimidis ◽

C Vlachopoulos ◽

C Georgakopoulos ◽

D Terentes-Printzios ◽

I Koutagiar ◽

...

Keyword(s):

Cigarette Smoking ◽

Tobacco Smoke ◽

Vascular Function ◽

Smoke Exposure ◽

Tobacco Smoke Exposure ◽

Smoking History ◽

Daily Smoking ◽

Microvascular Damage ◽

Smoking Intensity ◽

Smoking Exposure

Abstract Purpose Coronary artery disease death has been associated with increased cigarette smoking intensity. Aim of the study is to investigate the impact of cigarette smoking intensity on vascular function and structure changes among male smokers with similar age at starting smoking and moderate cumulative tobacco smoke exposure. Methods Indices of vascular function and structure including carotid-femoral pulse wave velocity (PWV), brachial flow-mediated dilation (bFMD), carotid intima media thickness (cIMT) and microvascular damage (penile vasculature) were measured in 118 smokers consuming up to 1 pack (20 cigarettes)/day and 58 patients smoking >1 pack (20 cigarettes)/day. The two groups had a similar mean cigarette smoking exposure (32 pack/years). Microvascular damage was examined by measuring penile peak systolic velocity (PSV) with a dynamic penile color Doppler ultrasonography after intracavernous injection of prostanglandin E1. Lower PSV values indicate severe penile vascular disease. Results The individuals smoking more than 1 pack/day were 10 years younger than smokers consuming up to 1 pack/day, however systolic, diastolic blood pressure, body-mass index, fasting blood glucose levels, lipid profile, C-reactive protein and total testosterone concentration were similar between the two groups. Figure shows mean bFMD, penile PSV, PWV and cIMT of the two groups. Interestingly, despite the similar cumulative smoking exposure between the two groups, the younger in age individuals with the intense cigarette smoking history had significantly lower mean bFMD and penile PSV (all P<0.05) and similar PWV and cIMT compared to the mean values of older subjects smoking up to 1 pack/day. Smoking intensity and vascular changes Conclusions Intense daily smoking accelerates damage of large arteries and significantly impairs microvascular and systemic endothelial function. Considering the predictive value of vascular biomarkers, the findings of this study imply the possibility that baseline daily smoking intensity could be a better summary measure of smoking-related cardiovascular risk among young heavy smokers, relative to total pack-years of smoking.

Download Full-text