Cigarette Smoke Exposure Inhibits Osteoclast Apoptosis via the mtROS Pathway

2021 ◽  
pp. 002203452110094
Author(s):  
Y. Qin ◽  
Y. Liu ◽  
Y. Jiang ◽  
S. Mei ◽  
Y. Liu ◽  
...  

It is widely known that smoking is a risk factor for bone loss and plays a key role in osteopenia. Despite this well-known association, the mechanisms by which smoking affects bone have not been definitively established. Since smoking increases bone loss and potentially affects bone resorption in response to mechanical force, we investigated the impact of cigarette smoke on osteoclast numbers and underlying mechanisms in a mouse model of orthodontic tooth movement (OTM). The experimental group was exposed to once-daily cigarette smoke while the control group was not, and tooth movement distance and osteoclast numbers were assessed. In addition, the effect of cigarette smoke extract (CSE) on osteoclast precursor proliferation and osteoclast apoptosis was assessed in vitro. We found that cigarette smoke exposure enhanced bone remodeling stimulated by mechanical force and increased osteoclast numbers in vivo. Also, CSE increased the number of osteoclasts by inhibiting osteoclast apoptosis via the mitochondrial reactive oxygen species/cytochrome C/caspase 3 pathway in vitro. Moreover, exposure of mice to cigarette smoke affected bone marrow cells, leading to increased formation of osteoclasts in vitro. This study identifies a previously unknown mechanism of how smoking has a detrimental impact on bone.

2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.


2020 ◽  
Vol 107 (1) ◽  
pp. 55-66
Author(s):  
B. Mammel ◽  
T. Kvárik ◽  
Zs. Szabó ◽  
J. Gyarmati ◽  
T. Ertl ◽  
...  

AbstractNumerous studies indicate that smoking during pregnancy exerts harmful effects on fetal brain development. The aim of this study was to determine the influence of maternal smoking during pregnancy on the early physical and neurobehavioral development of newborn rats. Wistar rats were subjected to whole-body smoke exposure for 2 × 40 min daily from the day of mating until day of delivery. For this treatment, a manual closed-chamber smoking system and 4 research cigarettes per occasion were used. After delivery the offspring were tested daily for somatic growth, maturation of facial characteristics and neurobehavioral development until three weeks of age. Motor coordination tests were performed at 3 and 4 weeks of age. We found that prenatal cigarette smoke exposure did not alter weight gain or motor coordination. Critical physical reflexes indicative of neurobehavioral development (eyelid reflex, ear unfolding) appeared significantly later in pups prenatally exposed to smoke as compared to the control group. Prenatal smoke exposure also resulted in a delayed appearance of reflexes indicating neural maturity, including hind limb grasping and forelimb placing reflexes. In conclusion, clinically relevant prenatal exposure to cigarette smoke results in slightly altered neurobehavioral development in rat pups. These findings suggest that chronic exposure of pregnant mothers to cigarette smoke (including passive smoking) results in persisting alterations in the developing brain, which may have long-lasting consequences supporting the concept of developmental origins of health and disease (DoHAD).


2020 ◽  
Vol 8 (1) ◽  
pp. 45
Author(s):  
Alfreda Sabrina Widyanti ◽  
Martha Ardiaria ◽  
Nurmasari Widyastuti

Background: Cigarette smoke exposure is one of the source of free radicals that causes oxidative stress and decreases superoxide dismutase (SOD) level. Purple fleshed sweet potato is a type of food that contains antioxidants to neutralize oxidative stress.Objectives: To study the effect of purple fleshed sweet potato on superoxide dismutase (sod) level on rats exposed to cigarette smoke.Methods: This was a true experimental study with a post-test randomized control group design. The rats were randomized into 4 groups (6 rats in each group). The negative control group (K-) was treated with standard diet; the positive control group (K+) was treated with cigarette smoke exposure and standard diet; the treatment 1 (P1) group was treated with standard diet and purple fleshed sweet potato with the dose of 8 g / 200 g bw/day, and the treatment 2 (P2) group was treated with cigarette smoke exposure and purple fleshed sweet potato with the dose of 8 g /200 g bw/day.Results: There was a significant difference of SOD levels in each group (p=0.00) except between group K- and P1. Giving purple fleshed sweet potatoes increased SOD levels as much as 85.81±4.59 (P1). The K+ group had the lowest SOD level 22.34±3.98. The SOD level for K- group and P2 group was 82.27±4.59 and 67.73±6.68 respectively.Conclusion: The highest SOD level is on the treatment 1 group which is administered with purple fleshed sweet potato.


2011 ◽  
Vol 5 (1) ◽  
Author(s):  
Jason Adamson ◽  
David Azzopardi ◽  
Graham Errington ◽  
Colin Dickens ◽  
John McAughey ◽  
...  

2018 ◽  
Vol 54 (1) ◽  
pp. 34
Author(s):  
Nyna Puspa Ningrum ◽  
Hermanto Tri Joewono ◽  
Widjiati Widjiati

Folic acid contains 5-methyltetrahydrofolate (5-MTHF), one of antioxidants that can be used to inhibit reaction caused by cigarette smoke exposure. Folic acid is able to inhibit the levels of Reactive Oxygen Species (ROS) so as to reduce the occurrence of neuronal apoptosis. The objectives of this study was to determine the effect of folic acid intake during pregnancy whose mother was exposed to cigarette smoke on brain neurons apoptosis index and quantity of mice (Mus musculus) offspring. This study was an experimental laboratory study with posttest-only control group design. The subjects were 24 female mice divided into 4 groups consisting of one control group and three treatment groups. Sampling used simple random sampling, each group consisting of 6 animals. Control group 1 was not given treatment during pregnancy, group 2 was given with folic acid orally on days 0-17 of gestational age as much as 0.06 mg/day/mice. Group 3 was given with cigarette smoke exposure on days 7-17 of gestational age, amounting to 2 cigarettes/day. Group 4 was given with cigarette smoke exposure on days 7-17 of gestational age, amounting to 2 cigarettes/day and folic acid orally on days 0-17 of gestational age as much as 0.06 mg/day/mice. The result showed significant differences in all variables. In neurons apoptosis index, there were significant differences between groups 1 and 3, groups 2 and 3, groups 3 and 4, significant differences in the quantity of neurons between groups 1 and 3, groups 2 and 3, groups 2 and 4. The study concluded that there were significant difference in neural apoptosis index between all groups, and there were also significant differences in the quantity of neurons between all groups.


Author(s):  
Endy Novryan Ridwan ◽  
Martono Tri Utomo ◽  
Harianto Notopuro

Introduction: This research aims to investigate and observe the effect of cigarette smoke exposure in the fetal growth and fetal development of mice (Mus musculus).  Methods: This was an experiment with post-test only control group design. The sample of the research was 36 pregnant mice which were randomly divided into 2 groups: control group (K) pregnant mice which inhaled ambient air without cigarette smoke exposure, and treatment group (P) pregnant mice which were given cigarette smoke exposure for 14 days with 2 bars of cigarette each day.  Results: The results showed a significant difference in the fetal birth weight between the group exposed to cigarette smoke (p < 0.05) compared with the control group. Fetal defect and stillbirth were not found in this research. Conclusion: The exposure of cigarette smoke gave negative effects of fetal growth and development because of the free radicals generated.


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