Smoking index, lifestyle factors, and genomic instability assessed by single-cell gel electrophoresis: a cross-sectional study in subjects from Yucatan, Mexico

Abstract

BackgroundIt is widely accepted that genomic instability is associated with several mechanisms involving oxidative stress, which can increase the rate of DNA breaks. Such factors include smoking, impairments in body composition, an unhealthy lifestyle, and a hereditary history of cancer. The aim was to evaluate the degree of association of genomic instability in smokers and non-smokers, and how the risk could change depending on the lifestyle and other causes. For this purpose, a survey of tobacco consumption, dietary patterns, physical activity, antecedents of cancer, and body composition assessment was carried out. Genomic instability was evaluated through a single-cell gel electrophoresis using peripheral blood mononuclear cells in three different conditions of oxidative stress. The analysis of genomic damage degree was performed through a dimension reduction procedure (principal component analysis) from 16 parameters per treatment (adding up 48 parameters of genomic damage per subject) and a binary logistic regression model for DNA fragmentation risk.ResultsThe sample consisted of 82 participants, divided into three age groups: young adults (18–35 years), adults (36–59 years), and older adults (60–95 years). As expected, the results showed a significant positive correlation of age with genomic damage rates, represented by 2 PCA groups (p = 0.027, p = 0.004). There were consistent significant positive associations of genomic damage rates with smoking index and three PCA groups (p = 0.007, p = 0.004, p = 0.009). The smoking status and age group analysis revealed that there were significant differences for adult smokers with the same aforementioned PCA groups (p = 0.002, p = 0.001, p = 0.010). In addition, higher DNA damage rates were found in subjects with incorrect diet patterns, long sitting hours, and previous exposure to radiation. The analysis with binary logistic regression displayed two models in which lifestyles (age, diet, and/or sedentarism) did not change the significance of smoking index for DNA fragmentation risk; however, when physical activity was present in the model, the smoking index was not a significant factor for DNA damage risk.ConclusionsAlthough it is well known that smoking affects human health in different ways, DNA fragmentation can be analyzed by a damage phenotypic analysis and integrate a risk analysis reshaped by diet and lifestyle in general.

The Influence of Environmental Polycyclic Aromatic Hydrocarbons (PAHs) Exposure on DNA Damage among School Children in Urban Traffic Area, Malaysia

“…Considering all children together, the present study revealed that children aged 10–11 years old had significantly higher tail moment compared to children aged 7 to 9 years old (3.03 ± 0.62 vs. 2.84 ± 0.71). Several studies have reported an increased DNA damage by older age as assessed by the comet assay [ 62 , 63 ]; meanwhile there are studies that showed no effect of age on the extent of DNA damage [ 64 , 65 ].…”

New Evidence of Microplastics in the Lower Respiratory Tract: Inhalation through Smoking

“…A smoking index was used to measure long-term tobacco consumption for each subject in the smoker group, which was calculated by the formula: (Daily smoking amount/ 20) × Smoking time. 30 Heavy smoking was defined as a smoking index ≥20 pack-years. The differences of statistics were tested using Mann−Whitney U tests for continuous variables and Fisher's tests for categorical variables.…”

“…For both groups, descriptive statistics were used to demonstrate the basic and clinical characteristics of the study population. A smoking index was used to measure long-term tobacco consumption for each subject in the smoker group, which was calculated by the formula: (Daily smoking amount/20) × Smoking time . Heavy smoking was defined as a smoking index ≥20 pack-years.…”

Daño del ADN como marcador potencial en el seguimiento clínico de pacientes femeninas con cáncer tratado

“…Cabe señalar al respecto que, dentro de este grupo, las que tuvieron el DB-N elevado fueron mayores de 25 años, y además todas habían estado expuestas a tratamientos con QTP y/o RTP. Si consideramos que diferentes factores pueden contribuir al daño del ADN, el incremento en las roturas de doble hebra pudiera deberse al efecto combinado de la edad, el tratamiento antineoplásico que recibieron, y la presencia de alguna susceptibilidad individual no identificada, que no implica a los APF-C, además de la dieta, el estilo de vida, la exposición ambiental, el metabolismo celular (11,30,31).…”

“…Por otra parte, la que presentaba Rb-B no recibió QTP y/o RTP. Como ya se ha mencionado, factores como la dieta, el estilo de vida, la exposición ambiental, el metabolismo celular (11,30), podrían estar relacionados con el incremento del DB-N en ellas. A su vez, la presencia de una susceptibilidad genética individual, también ya sugerida (26,27), podría estar in uenciando el daño del ADN.…”