347
Effect of Tobacco Smoking on Enzymatic and Metabolic
Pathways
The cigarette consists of heterogeneous cluster of exogenous compounds that can
restrict with several facets of endogenous hormones that interfere with various
human metabolic and enzymatic pathways. Recently, it has been obvious that metabolic disorders cannot be entirely attributed to enhance the caloric intake, deficit
sleep, and lack of physical activity and aging, among numerous environmental
factors are concerned to interrupt the metabolic pathways and cigarettes have
exhausted the utmost consideration of scientific community [3]. Throughout the
past 50 years, the worldwide rates of diabetes, obesity, and several others metabolic
and enzymatic disorders have been augmented exponentially. Actually, the predictable increases in the incidences of metabolic and enzymatic diseases coincide and
correlate chronically with an increase in cigarette use. Although, evolving epidemiological data are emphasizing the close relationship between cigarette smoke and
metabolic/enzymatic diseases. Animal and experimental data have proposed multiple pathways by which smoking can alter the hormonal environment and stimulate
metabolic disorders [21, 22]. Smoking mainly shown noxious impact during growth
and developmental duration like puberty, fetal life, progeny, pregnancy, infancy, and
menopause, can deleteriously affect the persons which suffer the crowd of metabolic, enzymatic, and several other diseases [3, 23].
Standard role of the endocrine system is reliant on hormonal/enzymatic pathway
which may act as chemical and biological messengers to regulate the physiological
functions of an organism. Similarly, glands are the source of hormone secretion and
then distribute it throughout the body with the help of carrier (blood and proteins)
and then the responses are showed by the action of enzyme on the target and specific
cells of the distant parts of the body. Smoking can affect the intracellular signaling,
enzymatic, hormonal, and metabolic pathways that could be functional under nongenomic and/or genomic mechanisms. As a non-genomic mechanism, binding of
hormone to receptor on surface of cell is considered responsible for triggering intercellular signal transduction as a result of smoking leading to deleterious effects [2].
Cigarette smoking poses a predictable risk to human health. Several studies
exhibit that genital malformation, diminishing sperm count, and elevating the deleterious/undesirable impact on reproduction caused by the disclosure of EDCs.
Increased utilization of cigarette not only alter the reproduction but also distress the
metabolism, persuade the onset of obesity, enzymatic and metabolic disorders.
Smoking can affect the morphological modification and alter the molecular and
enzymatic pathways. Cigarette smoke is also responsible to impair the regular metabolic pathway through interaction with members of superfamily of nuclear receptor
such as peroxisome proliferator activated receptor (PPAR), thyroid hormone
receptors(THR), farnesoid X receptor, liver X receptor, and retinoid X receptor [24].
Correspondingly, consumption of unclean water and food along with inhalation
of environmental airborne containments and impurities demonstrates the major concern of human contact to EDCs. Cigarette smoking that can un-suitably promote
20 Tobacco Smoking as an EDC in Metabolic Disorders
Effect of Tobacco Smoking on Enzymatic and Metabolic
Pathways
The cigarette consists of heterogeneous cluster of exogenous compounds that can
restrict with several facets of endogenous hormones that interfere with various
human metabolic and enzymatic pathways. Recently, it has been obvious that metabolic disorders cannot be entirely attributed to enhance the caloric intake, deficit
sleep, and lack of physical activity and aging, among numerous environmental
factors are concerned to interrupt the metabolic pathways and cigarettes have
exhausted the utmost consideration of scientific community [3]. Throughout the
past 50 years, the worldwide rates of diabetes, obesity, and several others metabolic
and enzymatic disorders have been augmented exponentially. Actually, the predictable increases in the incidences of metabolic and enzymatic diseases coincide and
correlate chronically with an increase in cigarette use. Although, evolving epidemiological data are emphasizing the close relationship between cigarette smoke and
metabolic/enzymatic diseases. Animal and experimental data have proposed multiple pathways by which smoking can alter the hormonal environment and stimulate
metabolic disorders [21, 22]. Smoking mainly shown noxious impact during growth
and developmental duration like puberty, fetal life, progeny, pregnancy, infancy, and
menopause, can deleteriously affect the persons which suffer the crowd of metabolic, enzymatic, and several other diseases [3, 23].
Standard role of the endocrine system is reliant on hormonal/enzymatic pathway
which may act as chemical and biological messengers to regulate the physiological
functions of an organism. Similarly, glands are the source of hormone secretion and
then distribute it throughout the body with the help of carrier (blood and proteins)
and then the responses are showed by the action of enzyme on the target and specific
cells of the distant parts of the body. Smoking can affect the intracellular signaling,
enzymatic, hormonal, and metabolic pathways that could be functional under nongenomic and/or genomic mechanisms. As a non-genomic mechanism, binding of
hormone to receptor on surface of cell is considered responsible for triggering intercellular signal transduction as a result of smoking leading to deleterious effects [2].
Cigarette smoking poses a predictable risk to human health. Several studies
exhibit that genital malformation, diminishing sperm count, and elevating the deleterious/undesirable impact on reproduction caused by the disclosure of EDCs.
Increased utilization of cigarette not only alter the reproduction but also distress the
metabolism, persuade the onset of obesity, enzymatic and metabolic disorders.
Smoking can affect the morphological modification and alter the molecular and
enzymatic pathways. Cigarette smoke is also responsible to impair the regular metabolic pathway through interaction with members of superfamily of nuclear receptor
such as peroxisome proliferator activated receptor (PPAR), thyroid hormone
receptors(THR), farnesoid X receptor, liver X receptor, and retinoid X receptor [24].
Correspondingly, consumption of unclean water and food along with inhalation
of environmental airborne containments and impurities demonstrates the major concern of human contact to EDCs. Cigarette smoking that can un-suitably promote
20 Tobacco Smoking as an EDC in Metabolic Disorders