Middle aged turn point in parameters of oxidative stress and glucose catabolism in mouse cerebellum during lifespan: minor effects of every-other-day fasting

2021 ◽  
Author(s):  
Maria M. Bayliak ◽  
Nadia M. Mosiichuk ◽  
Oksana M. Sorochynska ◽  
Oksana V. Kuzniak ◽  
Lesia O. Sishchuk ◽  
...  
Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Gratianne Rabiller ◽  
Atsushi Kanoke ◽  
Jialing Liu

Introduction: Previously we found that mice with type 2 diabetes (T2DM) exhibited an accelerated age-associated decline in neurogenesis during baseline and after ischemic stroke compared to age-matched control mice. The current study sought to delineate the transcriptome landscape involved in the impaired neurogenesis and determine if exercise can prevent the deleterious effect of T2DM on neural regeneration. Hypothesis: We hypothesize that T2DM alters signaling pathways regulating neurogenesis and daily exercise mitigates the deleterious effect on neurogenesis in the T2DM mice. Methods: Transcriptome profiling was performed by single cell RNA sequencing (scRNAseq) of SVZ and DG cells in stroke and non-stroke mice using the 10X Genomics platform. T2DM-induced differential gene expression was analyzed by ClusterProfiler and Wikipathways enrichment analysis. Middle-aged (~260 days old) and old (~700 days old) db/+ or db/db mice were subjected to daily wheel-running exercise for one month. BrdU at 50 mg/kg twice daily for 2 consecutive days was injected i.p. at the end of the experiment to track proliferating neuroprogenitor cells. DCX+ cells and BrDU+ cells were quantified in the dentate gyrus of the hippocampus. Results: The scRNAseq analysis revealed multiple cell types co-existing in the neurogenic niche. GO and Wikipathways enrichment analysis showed that under diabetic condition, genes such as Qdpr, Hsp90ab1, Hsp90aa1, and Sox9 were downregulated in pathways involving eNOS activation; whereas Junb, C1qc, C1qb and C1qa were upregulated in the pathways related to oxidative stress. Exercise, known to increase eNOS expression and reduce oxidative stress-induced cell death, significantly restored the number of DCX+ immature neurons in 8-months-old diabetic mice almost to the level of the control mice without exercise Conclusions: Exercise restores neurogenesis by increasing the number of neuroblasts in the middle-aged diabetic mice. Ongoing experiment will investigate whether exercise promotes neurogenesis by enhancing eNOS and improved blood flow, and inducing genes involved in the survival of the NSC niche of the diabetic mice.


2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Takuji Kawamura ◽  
Kumpei Tanisawa ◽  
Ryoko Kawakami ◽  
Chiyoko Usui ◽  
Tomoko Ito ◽  
...  

Previous studies have not investigated the determinants of resting oxidative stress, including physical fitness, as it relates to redox regulation. The present study therefore was aimed at identifying lifestyle and biological factors that determine resting oxidative stress, including objectively measured physical fitness. In 873 middle-aged and elderly men and women, age and anthropometric parameters, lifestyle-related parameters, medication and supplementation status, physical fitness, biochemical parameters, and nutritional intake status, as well as three plasma oxidative stress markers: protein carbonyl (PC), F2-isoprostane (F2-IsoP), and thiobarbituric acid reactive substances (TBARS), were surveyed and measured. The determinants of PC, F2-IsoP, and TBARS in all participants were investigated using stepwise multiple regression analysis. In PC, age ( β = − 0.11 , P = 0.002 ), leg extension power ( β = − 0.12 , P = 0.008 ), BMI ( β = 0.12 , P = 0.004 ), and HDL-C ( β = 0.08 , P = 0.040 ) were included in the regression model (adjusted R 2 = 0.018 ). In the F2-IsoP, smoking status ( β = 0.07 , P = 0.060 ), BMI ( β = 0.07 , P = 0.054 ), and HbA1c ( β = − 0.06 , P = 0.089 ) were included in the regression model (adjusted R 2 = 0.006 ). In TBARS, glucose ( β = 0.18 , P < 0.001 ), CRF ( β = 0.16 , P < 0.001 ), age ( β = 0.15 , P < 0.001 ), TG ( β = 0.11 , P = 0.001 ), antioxidant supplementation ( β = 0.10 , P = 0.002 ), and HbA1c ( β = − 0.13 , P = 0.004 ) were included in the regression model (adjusted R 2 = 0.071 ). In conclusion, the present study showed that age, anthropometric index, lifestyle-related parameters, medication and supplementation status, objectively measured physical fitness, biochemical parameters, and nutritional intake status explain less than 10% of oxidative stress at rest.


2019 ◽  
Vol 31 (6) ◽  
pp. 287-293
Author(s):  
Anders Jorgensen ◽  
Katrine Breitenstein ◽  
Otto Kalliokoski ◽  
Allan Weimann ◽  
Trine Henriksen ◽  
...  

AbstractObjective:Oxidative stress has been suggested to increase after electroconvulsive therapy (ECT), a treatment which continues to be the most effective for severe depression. Oxidative stress could potentially be mechanistically involved in both the therapeutic effects and side effects of ECT.Methods:We measured sensitive markers of systemic and central nervous system (CNS) oxidative stress on DNA and RNA (urinary 8-oxodG/8-oxoGuo, cerebrospinal fluid 8-oxoGuo, and brain oxoguanine glycosylase mRNA expression) in male rats subjected to electroconvulsive stimulations (ECS), an animal model of ECT. Due to the previous observations that link hypothalamic–pituitary–adrenal (HPA)-axis activity and age to DNA/RNA damage from oxidation, groups of young and middle-aged male animals were included, and markers of HPA-axis activity were measured.Results:ECS induced weight loss, increased corticosterone (only in middle-aged animals), and decreased cerebral glucocorticoid receptor mRNA expression, while largely leaving the markers of systemic and CNS DNA/RNA damage from oxidation unaltered.Conclusion:These results suggest that ECS is not associated with any lasting effects on oxidative stress on nucleic acids neither in young nor middle-aged rats.


Medicina ◽  
2008 ◽  
Vol 44 (5) ◽  
pp. 392 ◽  
Author(s):  
Liucija Černiauskienė ◽  
Dalia Lukšienė ◽  
Abdonas Tamošiūnas ◽  
Regina Rėklaitienė ◽  
Lilija Margevičienė

The aim of this study was to evaluate the association of metabolic syndrome and oxidative stress with ischemic heart disease in middle-aged persons (men and women aged 45–64 years). Material and methods. In this study, we have used data of 533 persons (247 men and 286 women) aged 45– 64 years from Kaunas population cohort investigated according to WHO MONICA study protocol during 2001–2002 in whom concentrations of malondialdehyde, a marker of lipid peroxidation, and antioxidant vitamin E in blood serum were determined. Metabolic syndrome was defined by the criteria of Adult Treatment Panel III. Oxidative stress was determined in the presence of increased level of malondialdehyde (≥5 mmol/L) and decreased level of lipid-standardized vitamin E (<20 mmol/L). The levels of malondialdehyde and vitamin E were measured by fluorimetric methods. Results. Ischemic heart disease was diagnosed in 19.8% of men and 21.3% of women. The frequency of ischemic heart disease among persons (men and women) with metabolic syndrome was significantly higher than among persons without metabolic syndrome (27.4% vs. 17.8%, respectively; odds ratio, 1.63; P=0.032). The frequency of ischemic heart disease among persons with oxidative stress was significantly higher than among persons without oxidative stress (29.1% vs. 17.6%, respectively; odds ratio, 1.88; P=0.029). The highest prevalence of ischemic heart disease (30.0%) was among persons with metabolic syndrome and oxidative stress, and the lowest prevalence of this disease (13.8%) was among persons without metabolic syndrome and without oxidative stress (odds ratio, 2.54; P=0.017). These data were adjusted by sex and age. Conclusion. Metabolic syndrome and oxidative stress are significantly associated with ischemic heart disease among 45–64-year-old persons.


2019 ◽  
Vol 35 (7) ◽  
pp. 586-590 ◽  
Author(s):  
C. P. Teixeira ◽  
R. Florencio-Silva ◽  
G. R. S. Sasso ◽  
A. A. F. Carbonel ◽  
R. S. Simões ◽  
...  

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