Spatially-integrated estimates of net ecosystem exchange and methane fluxes from Canadian peatlands.

BACKGROUND: Peatlands are an important component of Canada's landscape, however there is little information on their national-scale net emissions of carbon dioxide [Net Ecosystem Exchange (NEE)] and methane (CH4). This study compiled results for peatland NEE and CH4 emissions from chamber and eddy covariance studies across Canada. The data were summarized by bog, poor fen and rich-intermediate fen categories for the seven major peatland containing terrestrial ecozones (Atlantic Maritime, Mixedwood Plains, Boreal Shield, Boreal Plains, Hudson Plains, Taiga Shield, Taiga Plains) that comprise > 96% of all peatlands nationally. Reports of multiple years of data from a single site were averaged and different microforms (e.g., hummock or hollow) within these peatland types were kept separate. A new peatlands map was created from forest composition and structure information that distinguishes bog from rich and poor fen. National Forest Inventory k-NN forest structure maps, bioclimatic variables (mean diurnal range and seasonality of temperatures) and ground surface slope were used to construct the new map. The Earth Observation for Sustainable Development map of wetlands was used to identify open peatlands with minor tree cover. RESULTS: The new map was combined with averages of observed NEE and CH4 emissions to estimate a growing season integrated NEE (± SE) at - 108.8 (± 41.3) Mt CO2 season-1 and CH4 emission at 4.1 (± 1.5) Mt CH4 season-1 for the seven ecozones. Converting CH4 to CO2 equivalent (CO2e; Global Warming Potential of 25 over 100 years) resulted in a total net sink of - 7.0 (± 77.6) Mt CO2e season-1 for Canada. Boreal Plains peatlands contributed most to the NEE sink due to high CO2 uptake rates and large peatland areas, while Boreal Shield peatlands contributed most to CH4 emissions due to moderate emission rates and large peatland areas. Assuming a winter CO2 emission of 0.9 g CO2 m-2 day-1 creates an annual CO2 source (24.2 Mt CO2 year-1) and assuming a winter CH4 emission of 7 mg CH4 m-2 day-1 inflates the total net source to 151.8 Mt CO2e year-1. CONCLUSIONS: This analysis improves upon previous basic, aspatial estimates and discusses the potential sources of the high uncertainty in spatially integrated fluxes, indicating a need for continued monitoring and refined maps of peatland distribution for national carbon and greenhouse gas flux estimation.

Genetic susceptibility of glutathione S-transferase genes (GSTM1/T1 and P1) to coronary artery disease in Asian Indians.

Genetic polymorphisms in glutathione S-transferase (GST) genes may modulate the risk of cardiovascular diseases. The objective of present study was to investigate the potential association between the polymorphisms of GSTM1/T1 and P1 genes and their influence on diverse clinical parameters and oxidative stress biomarkers in coronary artery disease (CAD) patients in Asian Indians. The present study includes 562 angiographically confirmed CAD patients and 564 healthy control subjects from the north Indian population. Anthropometric and clinical measurements were performed for all the participants. The oxidative stress biomarkers including malondialdehyde and total antioxidant capacity were also measured. The genotyping of the GSTM1/T1 and P1 genes was performed using the multiplex-PCR and PCR-RFLP methods. The CAD patients exhibit significantly high values of waist circumference, waist-to-hip ratio, body fat (%), glucose, triglycerides, and very low-density lipoprotein, and reduced high-density lipoprotein levels compared to control subjects (P < 0.001). Malondialdehyde levels were significantly enhanced, and the total antioxidant capacity was reduced in CAD patients compared to controls (P < 0.001). However, no significant difference in body mass index and total cholesterol levels were observed in CAD patients and control subjects. The frequencies of the GSTM1 and GSTM1/T1 null genotypes in the CAD patients were significantly higher than the control subjects. In contrast, the GSTT1(-) genotype frequencies were significantly lower in CAD patients than the controls. Logistic regression analysis of the data revealed the null genotype of GSTM1 and the GG genotype of the GSTP1 (313A/G) gene were associated with an approximately twofold enhanced risk of developing CAD, whereas GSTT1(-) plays a defensive role against CAD development in north Indians. Upon stratification of data according to the genotypes of the GSTM1/T1 and P1 genes, we did not find significant a difference among the various metabolic traits in CAD patients and controls. Our results suggest that oxidative damage induced by lipid peroxidation with reduced antioxidant capacity and genetic variants in GST genes (GSTM1/T1 and P1) may modify the risk of CAD development in Asian Indian population.

Implications of ACE (I/D) Gene Variants to the Genetic Susceptibility of Coronary Artery Disease in Asian Indians.

Angiotensin-1-converting enzyme (ACE) gene has established substantial attention in the recent years as a candidate gene for hypertension, cardiovascular diseases and type 2 diabetes. The aim of the present study was to investigate the association of ACE (I/D) polymorphism with coronary artery disease (CAD) in a north Indian population. A total of 662 subjects (330 CAD patients and 332 healthy controls) were examined for association of ACE gene (I/D) polymorphism and environmental risk factors. The mean age of the CAD patients and control subjects was 60.53 ± 8.6 years and 56.55 ± 7.7 years, respectively (p = 0.000). Anthropometric and demographic data showed BMI values significantly higher among CAD patients and control subjects (26.98 ± 4.9 vs 24.04 ± 4.7, p = 0.000). We observed pronounced central obesity in both CAD patients and controls, even at the lowest BMI values (<23 kg/m2). Dyslipidemia was highly prevalent in CAD patients compared to control subjects. Genotypic data showed significantly higher frequency of DD genotype in CAD patients than that of control subjects (40 vs 28.3 %). No significant difference was observed in the distribution of ID genotypes between CAD patients and control subjects. Logistic regression analysis of data demonstrate that DD genotype was associated with 1.8 fold increased risk of development of CAD in Asian Indians (OR 1.8; 95 % CI 1.22-2.66; p = 0.003). The frequency of D allele was significantly higher in CAD patients (p = 0.001). No significant difference was observed in the clinical and biochemical characteristics of CAD patients and controls when the data was stratified according to the genotypes of ACE gene. In conclusion, DD genotype of ACE gene may be associated with increased risk of CAD in Asian Indian population.

MicroRNAs, Aging, Cellular Senescence, and Alzheimer's Disease.

Aging is a normal process of living being. It has been reported that multiple cellular changes, including oxidative damage/mitochondrial dysfunction, telomere shortening, inflammation, may accelerate the aging process, leading to cellular senescence. These cellular changes induce age-related human diseases, including Alzheimer's, Parkinson's, multiple sclerosis, amyotrophic lateral sclerosis, cardiovascular, cancer, and skin diseases. Changes in somatic and germ-line DNA and epigenetics are reported to play large roles in accelerating the onset of human diseases. Cellular mechanisms of aging and age-related diseases are not completely understood. However, recent discoveries in molecular biology have revealed that microRNAs (miRNAs) are potential indicators of aging, cellular senescence, and Alzheimer's disease (AD). The purpose of our chapter is to highlight recent advancements in miRNAs and their involvement in cellular changes in aging, cellular senescence, and AD. This chapter also critically evaluates miRNA-based therapeutic drug targets for aging and age-related diseases, particularly Alzheimer's.

Therapeutic Strategies for Mitochondrial Dysfunction and Oxidative Stress in Age-Related Metabolic Disorders.

Mitochondria are complex, intercellular organelles present in the cells and are involved in multiple roles including ATP formation, free radicals generation and scavenging, calcium homeostasis, cellular differentiation, and cell death. Many studies depicted the involvement of mitochondrial dysfunction and oxidative damage in aging and pathogenesis of age-related metabolic disorders and neurodegenerative diseases. Remarkable advancements have been made in understanding the structure, function, and physiology of mitochondria in metabolic disorders such as diabetes, obesity, cardiovascular diseases, and stroke. Further, much progress has been done in the improvement of therapeutic strategies, including lifestyle interventions, pharmacological, and mitochondria-targeted therapeutic approaches. These strategies were mainly focused to reduce the mitochondrial dysfunction caused by oxidative stress and to retain the mitochondrial health in various diseases. In this chapter, we have highlighted the involvement of mitochondrial dysfunction in the pathophysiology of various disorders and recent progress in the development of mitochondria-targeted molecules as therapeutic measures for metabolic disorders.

MicroRNAs as Peripheral Biomarkers in Aging and Age-Related Diseases.

MicroRNAs (miRNAs) are found in the circulatory biofluids considering the important molecules for biomarker study in aging and age-related diseases. Blood or blood components (serum/plasma) are primary sources of circulatory miRNAs and can release these in cell-free form either bound with some protein components or encapsulated with microvesicle particles, called exosomes. miRNAs are quite stable in the peripheral circulation and can be detected by high-throughput techniques like qRT-PCR, microarray, and sequencing. Intracellular miRNAs could modulate mRNA activity through target-specific binding and play a crucial role in intercellular communications. At a pathological level, changes in cellular homeostasis lead to the modulation of molecular function of cells; as a result, miRNA expression is deregulated. Deregulated miRNAs came out from cells and frequently circulate in extracellular body fluids as part of various human diseases. Most common aging-associated diseases are cardiovascular disease, cancer, arthritis, dementia, cataract, osteoporosis, diabetes, hypertension, and neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Variation in the miRNA signature in a diseased peripheral circulatory system opens up a new avenue in the field of biomarker discovery. Here, we measure the biomarker potential of circulatory miRNAs in aging and various aging-related pathologies. However, further more confirmatory researches are needed to elaborate these findings at the translation level.

Molecular Links and Biomarkers of Stroke, Vascular Dementia, and Alzheimer's Disease.

Stroke is a very common neurological disease, and it occurs when the blood supply to part of the brain is interrupted and the subsequent shortage of oxygen and nutrients causes damage to the brain tissue. Stroke is the second leading cause of death and the third leading cause of disability-adjusted life years. The occurrence of stroke increases with age, but anyone at any age can suffer a stroke. Stroke can be broadly classified in two major clinical types: ischemic stroke (IS) and hemorrhagic stroke. Research also revealed that stroke, vascular dementia (VaD), and Alzheimer's disease (AD) increase with a number of modifiable factors, and most strokes can be prevented and/or controlled through pharmacological or surgical interventions and lifestyle changes. The pathophysiology of stroke, VaD, and AD is complex, and recent molecular and postmortem brain studies have revealed that multiple cellular changes have been implicated, including inflammatory responses, microRNA alterations, and marked changes in brain proteins. These molecular and cellular changes provide new information for developing therapeutic strategies for stroke and related vascular disorders treatment. IS is the major risk factor for VaD and AD. This chapter summarizes the (1) links among stroke-VaD-AD; (2) updates the latest developments of research in identifying protein biomarkers in peripheral and central nervous system tissues; and (3) critically evaluates miRNA profile and function in human blood samples, animal, and postmortem brains.

Alterations in Ca²âº homeostasis and oxidative damage induced by ethion in erythrocytes of Wistar rats: ameliorative effect of vitamin E.

Organophosphate (OP) insecticides have been reported to induce oxidative stress due to lipid peroxidation and alteration in defense mechanisms. It is known that calcium content in erythrocytes plays a very important in normal physiology of cells. Erythrocytes are a very convenient model to understand the susceptibility of membrane to oxidative damage induced by various xenobiotic compounds. The aim of present study was to investigate the effects of ethion induced oxidative damage, alterations in membrane bound enzymes and Ca(2+) homeostasis and a possible protective role of vitamin E. Adult male albino rats of Wistar strain were orally administered ethion and vitamin E daily for 28 days. Animals were randomly divided into four groups: control; ethion treated (2.7 mg/kgbw/day); vitamin E treated (50mg/kg of bw/day); ethion+vitamin E treated. The animals were sacrificed after 7, 14, 21 and 28 days. Erythrocyte membranes were prepared and analyzed for protein, lipid peroxidation (LPO) and membrane bound ATPases. Furthermore, Ca(2+) homeostasis as function of time and concentration was evaluated in erythrocytes. The results from the present study show that in vivo administration of ethion resulted in oxidative damage to erythrocyte membranes as evident by increased lipid peroxidation. The increased LPO following ethion intoxication was accompanied by significant decrease in the activities of Na(+)/K(+)-ATPase, Mg(2+)-ATPase and Ca(2+)-ATPase and disturbed Ca(2+)homeostasis in erythrocytes. Furthermore, vitamin E treatment had a beneficial effect by decreasing lipid peroxidation; partially restoring activities of membrane bound ATPases and Ca(2+) homeostasis. The present study suggests that ethion exerts its toxic effect by increasing LPO, altering the activity of membrane bound enzymes and disturbing Ca(2+) homeostasis. Vitamin E treatment ameliorated the toxic effects of ethion suggesting its role as a potential antioxidant.

Ameliorative action of melatonin on oxidative damage induced by atrazine toxicity in rat erythrocytes.

Excessive generation of reactive oxygen species (ROS) can induce oxidative damage to vital cellular molecules and structures including DNA, lipids, proteins, and membranes. Recently, melatonin has attracted attention because of their free radical scavenging and antioxidant properties. The aim of this study was to evaluate the possible protective role of melatonin against atrazine-induced oxidative stress in rat erythrocytes in vivo. Adult male albino rats of Wistar strain were randomly divided into four groups. Control group received isotonic saline; melatonin (10 mg/kg bw/day) group; atrazine (300 mg/kg of bw/day) group; atrazine + melatonin group. Oral administration of atrazine and melatonin was given daily for 21 days. Oxidative stress was assessed by determining the glutathione (GSH) and malondialdehyde (MDA) level, and alteration in antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione-S-transferase (GST), and glucose-6-phosphate dehydrogenase (G-6-PD) in the erythrocytes of normal and experimental animals. A significant increase in the MDA levels and decrease in the GSH was observed in the atrazine treated animals (P < 0.05). Also, significant increase in the activities of SOD, CAT, GPx, and GST were observed in atrazine treated group compared to controls (P < 0.05). Moreover, significant decrease in protein, total lipids, cholesterol, and phospholipid content in erythrocyte membrane were demonstrated in atrazine treated rats. Administration of atrazine significantly inhibits the activities of G-6-PD and membrane ATPases such as Na(+)/K(+)-ATPase, Mg(2+)-ATPase, and Ca(2+)-ATPase (P < 0.05). Scanning electron microscopic (SEM) examination of erythrocytes revealed morphological alterations in the erythrocytes of atrazine treated rats. Furthermore, supplementation of melatonin significantly modulates the atrazine-induced changes in LPO level, total lipids, total ATPases, GSH, and antioxidant enzymes in erythrocytes. In conclusion, the increase in oxidative stress markers and the concomitant alterations in antioxidant defense system indicate the role of oxidative stress in erythrocytes of atrazine-induced damage. Moreover, melatonin shows a protective role against atrazine-induced oxidative damage in rat erythrocytes.

Biochemical and morphological perturbations in rat erythrocytes exposed to ethion: protective effect of vitamin E.

Erythrocyte membranes are an excellent model system to study interaction of pro-oxidants with membranes. The aim of the present study is to examine the effect of vitamin E on ethion-induced biochemical and morphological alterations in erythrocytes. Ethion was administered to the rats orally at a daily dose of 2.7 mg/kg body weight for a period of 7, 14, 21 and 28 days. The results from the present study show that administration of ethion resulted in oxidative damage to erythrocyte membranes as evident by increased lipid peroxidation and decreased phospholipid content. This was accompanied by decrease in membrane cholesterol levels. In addition, ethion exposure inhibited the activities of membrane bound enzymes; Na+ K+ ATPase and Mg2+ATPase. Scanning electron micrographs of erythrocytes from animals exposed to ethion revealed morphological changes. Supplementation of vitamin E (50 mg/kg body weight) to ethion exposed animals ameliorated the ethion-induced oxidative stress, restored membrane lipid composition and activity of membrane bound enzymes along with erythrocyte shape. The results clearly demonstrate that ethion-induced damage involves increase in oxidative stress that results in alterations in erythrocyte membrane structure and function. Furthermore, supplementation with vitamin E reversed ethion induced alterations suggesting its beneficial role in individuals exposed to ethion.