Study Of The Biological Damage Effect Of Subchronic Smoking Exposure Of Rats

[Objective]Smoking and passive smoking can lead to cardiovascular and cerebrovascular diseases, respiratory diseases, multi-site cancer, and other diseases, in order to clarify the pathogenesis of smoking, more and more research dedicated to finding biological exposure markers and effect biomarkers. This study was conducted on rats by cigarette smoke subchronic exposure, detected effects of exposure to assess of early biological effects. To analyze of early biological effects of damage and dose-response relationship of smoke exposure.[Methods](1) Wistar rats were exposed to cigarette smoke with using dynamic smoke exposure apparatus. Animals inhaled cigarette smoke with constant oxygen, constant pressure, constant humidity and a constant temperature and uniform conditions. By exposed subchronic systemic exposure, to establish an animal model of exposure.(2) 160 SPF Wistar rats (♂:220-250 g;♀:180-220 grams each 80) were selected.Randomized into the lowgroup (LM, flue gas concentration of 10%), middlegroup (MM, gas concentration of 20%), high group (HM, gas concentration of 60%) and control group (CM).Cigarette smoke exposure for 3 months, each group were 15 male and 15 female rats, exposure time of 30 minutes. Cigarette smoke exposure for 6 months, each group were 5 male and 5 female rats, exposure time 30 minutes. (3)Detecting the cotinine of rat urine by GS-MS.(4) Take the left lung tissue in rats, fixed in 10% formalin and do Pathological Analysis.(5) After washing the right lung with PBS, cryopreservation, detected of markers of inflammation and oxidative stress parameters with by using Elisa.(6)Detected serum biochemical indices.[Results](1) The exposed groups (LM,MM,HM) compared with the control group, weight trending in male rats was significantly different (P<0.001), weight gain was lower than the control group.(2)Cigarette smoke exposure for 3 months, the exposed groups (MM,HM) compared with the control group,heart weight ratio was significantly different(P<0.05); the exposed groups (MM) compared with the control group, renal weight ratio was significantly different(P<0.01);the exposed groups (MF) compared with the control group, liver weight ratio was significantly different(P<0.05).Cigarette smoke exposure for 6 months, the exposed groups (MM,HM) compared with the control group liver weight ratio was significantly different(P<0.05);the exposed groups (MF) compared with the control group, heart weight ratio was significantly different(P<0.01);the exposed groups (MF) compared with the control group, liver weight ratio was significantly different(P<0.05).(3)The exposed groups (LM,MM,HM) compared with the control group, cotinine concentration of rat urine was significantly different(P<0.01). (4)Detected sera, compared with the control group, ALT、AST、ALP、TG and LDH weresignificantly different(P<0.05).(5)Compared with the control group, GSHMDA、TNF-a、TGF-b、IL-1 and IL-6 weresignificantly different.(6)The exposed groups compared with the control group, rat alveolar size uneven, some alveolar septal thinning or rupture, appear goblet cell hyperplasia in varying degrees, have seen significant inflammatory cell infiltration, and as the exposure dose increases, more and more obvious lung inflammation.[Conclusion](1) Established the animal modelfor rats exposed to cigarette smoke subchronic exposure.in establishment of a sub-chronic exposure to cigarette smoke toxicity rat animal model, sub-chronic cigarette smoke exposure on growth trends in male rats significant weight.Subchronic cigarette smoke exposure on weight growth trends in male rats was significant different.(2) With increasing doses of exposure to smoke, the cotininecontent in rat urinesignificantly. It prove that the main metabolite of nicotine concentrationcanbe ratherreflect smoke intake of the nicotine and other harmful components. It can be an effective marker for exposure to cigarette smoke.(3) The comparison between the exposed groups and control group exposed to organs.weight ratio,blood biochemistry,lung inflammation indicators of oxidative stress, and found that cigarette smoke exposure can cause sub-chronic rat heart, liver and kidney function was significantly affected, cause the lung obvious inflammation and oxidative damage. Smoke exposure on rat heart, liver, kidneys, lungs are causing biological damage, and exposure with increasing dose, damage effect increased.