The objective of the present study was to use the comet assay to evaluate the steady-state level of DNA damage in peripheral blood leukocytes from diabetic and non-diabetic female Wistar rats exposed to air or to cigarette smoke. A total of 20 rats were distributed into four experimental groups (n=5 rats/group): non-diabetic (control) and diabetic exposed to filtered air; non-diabetic and diabetic exposed to cigarette smoke. A pancreatic beta (beta)-cytotoxic agent, streptozotocin (40 mg/kg b.w.) was used to induce experimental diabetes in rats. Rats placed into whole-body exposure chambers were exposed for 30 min to filtered air (control) or to tobacco smoke generated from 10 cigarettes, twice a day, for 2 months. At the end of the 2-month exposure period, each rat was anesthetized and humanely killed to obtain blood samples for genotoxicity analysis using the alkaline comet assay. Blood leukocytes sampled from diabetic rats presented higher DNA damage values (tail moment=0.57+/-0.05; tail length=19.92+/-0.41, p<0.05) compared to control rats (tail moment=0.34+/-0.02; tail length=17.42+/-0.33). Non-diabetic (tail moment=0.43+/-0.04, p>0.05) and diabetic rats (tail moment=0.41+/-0.03, p>0.05) exposed to cigarette smoke presented non-significant increases in DNA damage levels compared to control group. In conclusion, our data show that the exposure of diabetic rats to cigarette smoke produced no additional genotoxicity in peripheral blood cells of female Wistar rats.
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http://dx.doi.org/10.1016/j.mrgentox.2006.12.004 | DOI Listing |
Int Forum Allergy Rhinol
January 2025
Division of Division of Rhinology & Skull Base Surgery Department of Otolaryngology, University of Florida, Gainesville, Florida, USA.
Rationale: Smoking has been shown to be associated with circulating deficiencies in 25(OH)D3 and reduced sinonasal tissue levels of the active form of vitamin D, 1,25(OH)2D3. Given vitamin D's ability to reduce inflammation, we sought to examine if intranasal (IN) delivery of calcitriol [clinical analog of 1,25(OH)2D3] could reduce inflammation and improve disease severity in a murine model of chronic cigarette smoke-induced sinonasal inflammation (CS-SI).
Methods: Mice were exposed to CS 5 h/day, 5 days/week for 9 months, and then began IN calcitriol three times per week for 4 weeks.
Lancet Reg Health Southeast Asia
January 2025
British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
Background: South Asians may be particularly susceptible to premature myocardial infarction (MI) owing both to conventional cardiovascular risk factors and practices distinctive to South Asia. Identifying modifiable risk factors for MI in these populations could inform prevention strategies. We have, therefore, studied conventional risk factors and other characteristics in relation to occurrence of first MI in Bangladesh.
View Article and Find Full Text PDFHeliyon
January 2025
School of Public Health, University of Alberta, 11405 87 Ave NW, Edmonton, Alberta, T6G 1C9, Canada.
Background: Based on the socio-ecological model of health, socioeconomic policy is an important determinant of population health. Spending decisions by public health units (PHU) have been shown to be associated with population health outcomes. Some studies have found greater PHU spending to be associated with improved population health, while others report mixed findings, warranting further research.
View Article and Find Full Text PDFCureus
December 2024
Department of Surgery, Arabian Gulf University, Manama, BHR.
Periductal mastitis (PM) is a form of nonlactational mastitis. The clinical picture varies from mild periareolar inflammation to frank retroareolar abscess formation. A huge amount of literature is incriminating cigarette smoking as a major contributing factor to the etiology of PM, and cessation of smoking is essential for a successful treatment.
View Article and Find Full Text PDFHealth Econ
January 2025
Centro de Investigaciones Económicas y Empresariales, Universidad Privada Boliviana, La Paz, Bolivia.
In this research we show that ambitious increases in tobacco tax rates can substantially reduce tobacco consumption, increase fiscal revenue, and provide net positive social benefits even in contexts of low consumption prevalence and intensity. Low nicotine intake still constitutes a grave disease risk factor, and the effectiveness of tax increases might be questioned if income effects are small. We adapt spatial variation of price methodologies to deal with low prevalence and intensity, censored data, and small samples using the Bolivian case as an illustration.
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