Accelerated senescence in kidneys of low-birth-weight rats after catch-up growth

2009 ◽  
Vol 297 (6) ◽  
pp. F1697-F1705 ◽  
Author(s):  
Valerie A. Luyckx ◽  
Catharine A. Compston ◽  
Thomas Simmen ◽  
Thomas F. Mueller
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiovascular Disease ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Normal Birth Weight ◽  
Normal Birth ◽  
Catch Up

Epidemiological studies show a strong association between low birth weight and hypertension, renal, and cardiovascular disease, especially after catch-up growth. Senescence is an important contributor to the progression of chronic disease. Developmentally programmed premature senescence may be a link among low birth weight, catch-up growth, and adult disease. Low birth weight was induced by feeding pregnant rats a low-protein diet from day 12 of gestation to 10 days postdelivery. Low- and normal-birth-weight male offspring were weaned onto regular or high-calorie diets to enhance catch-up growth. Kidneys and hearts of offspring were analyzed for RNA and protein markers of stress-induced senescence (p16, p21, p53, Rb). Markers of mitochondrial stress (p66Shc) and activation of endoplasmic reticulum protein secretion (Ero1α) were analyzed as regulators of reactive oxygen species generation. Reactive oxygen species are known to be associated with premature aging. Senescence markers were not different in low- or normal-birth-weight kidneys at birth. During rapid catch-up growth, p16 and p21 increased significantly in low-birth-weight kidneys and hearts ( P < 0.01). Renal p16 levels increased progressively and were significantly higher in low-birth-weight kidneys at 3 and 6 mo ( P ≤ 0.02). Renal p66Shc and Ero1α were significantly higher in low- compared with normal- birth-weight kidneys at 6 mo, suggesting reactive oxygen species generation ( P ≤ 0.03). Low-birth-weight rats exhibit accelerated senescence in kidneys and hearts after rapid catch-up growth, a likely important link between early growth and subsequent hypertension, renal, and cardiovascular disease.

MORTALITY FROM CONGENITAL CARDIOVASCULAR DISEASE IN OREGON

PEDIATRICS ◽  
1967 ◽  
Vol 40 (3) ◽  
pp. 334-344
Author(s):  
Victor D. Menashe ◽  
Harold T. Osterud ◽  
Herbert E. Griswold
Keyword(s):  
Cardiovascular Disease ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Life Span ◽  
Normal Birth Weight ◽  
Parental Age ◽  
Cardiac Malformation ◽  
Death Rates ◽  
Normal Birth ◽  
Weight One

Over one half of the deaths from all congenital malformations were due to congenital cardiovascular disease. There were 496 individuals who died of congenital cardiovascular disease in Oregon during 1957 thru 1961, and three fourths of the deaths occurred in infants under 1 year of age. More males were affected by congenital cardiovascular disease than females, but, when congenital cardiovascular disease was present, the length of survival, as measured by life span, did not differ by sex. One out of every four infants dying of congenital cardiovascular disease was of low birth weight; of these, 60% were over 37 weeks' gestation. However, there was no difference in the life span of low birth weight and normal birth weight infants who died with congenital cardiovascular disease. This would imply that the significant factor of death in these infants was the cardiac malformation rather than the low birth weight. One out of every three infants who died with congenital cardiovascular disease had malformations of other systems. Fewer deaths than expected were identified among first born. Fetal deaths were noted more frequently in the population of mothers of children with congenital heart disease than in the overall population. The parental age in this group was significantly higher than in the general population and death rates of infants with congenital cardiovascular disease increased with advancing parental age. Thirty-two percent of the infants who died with congenital cardiovascular disease had single lesions. Early diagnosis and treatment is to be stressed if mortality is to be reduced.

Роль оксида азота в реализации антиоксидантного эффекта неопиатного аналога лей-энкефалина в сердце новорожденных белых крыс

2019 ◽  
pp. 61-64
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Postnatal Period ◽  
Oxide System ◽  
No Synthase ◽  
Albino Rats ◽  
Oxygen Species ◽  
Control Parameters ◽  
Synthase Inhibitor

The eff ect of the non-opiate analog of leu-enkephalin (peptide NALE: Phe – D – Ala – Gly – Phe – Leu – Arg) on the reactive oxygen species generation in the heart of albino rats in the early postnatal period was studied. Peptide NALE was administered intraperitoneally in the dose of 100 μ/kg daily from 2 to 6 days of life. Reactive oxygen species generation was assessed by chemiluminescence in the heart homogenates of 7-day-old animals. Decreasing of reactive oxygen species generation nearly by 30 % and an increasing in antioxidant system activity by the 20-27 %, compared with the control parameters, were found. The antioxidant eff ect of peptide NALE is associated with the presence of the amino acid Arg in the structure of the peptide. An analogue of NALE peptide, devoid of Arg (peptide Phe – D – Ala – Gly – Phe – Leu – Gly), had a signifi cant lower antioxidant eff ect. The NO-synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in the dose 50 mg/kg, administered with NALE peptide, reduced the severity of the NALE antioxidant eff ect. The results of the study suggest that the pronounced antioxidant eff ect of NALE peptide in the heart of albino rats, at least in part, is due to the interaction with the nitric oxide system.

Stimulated Reactive Oxygen Species Generation in the Spermatozoa of Infertile Men

1993 ◽  
Vol 149 (1) ◽  
pp. 64-67 ◽  
Author(s):  
Donald L. Weese ◽  
Michael L. Peaster ◽  
Kyle K. Himsl ◽  
Gary E. Leach ◽  
Pramod M. Lad ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Infertile Men

scholarly journals Melatonin Induces Melanogenesis in Human SK-MEL-1 Melanoma Cells Involving Glycogen Synthase Kinase-3 and Reactive Oxygen Species

2020 ◽  
Vol 21 (14) ◽  
pp. 4970
Author(s):  
Juan Perdomo ◽  
Carlos Quintana ◽  
Ignacio González ◽  
Inmaculada Hernández ◽  
Sara Rubio ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Glycogen Synthase ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Glycogen Synthase Kinase ◽  
Oxygen Species ◽  
Glycogen Synthase Kinase 3Β ◽  
Human Melanoma Cells

Melatonin is present in all living organisms where it displays a diversity of physiological functions. Attenuation of melanogenesis by melatonin has been reported in some mammals and also in rodent melanoma cells. However, melatonin may also stimulate melanogenesis in human melanoma cells through mechanisms that have not yet been revealed. Using the human melanoma cells SK-MEL-1 as a model, an increase in both tyrosinase activity and melanin was already observed at 24 h after melatonin treatment with maximal levels of both being detected at 72 h. This effect was associated with the induction in the expression of the enzymes involved in the synthesis of melanin. In this scenario, glycogen synthase kinase-3β seems to play a significant function since melatonin decreased its phosphorylation and preincubation with specific inhibitors of this protein kinase (lithium or BIO) reduced the expression and activity of tyrosinase. Blocking of PI3K/AKT pathway stimulated melanogenesis and the effect was suppressed by the inhibitors of glycogen synthase kinase-3β. Although melatonin is a recognized antioxidant, we found that it stimulates reactive oxygen species generation in SK-MEL-1 cells. These chemical species seem to be an important signal in activating the melanogenic process since the antioxidants N-acetyl-l-cysteine and glutathione decreased both the level and activity of tyrosinase stimulated by melatonin. Our results support the view that regulation of melanogenesis involves a cross-talk between several signaling pathways.

Antioxidant Levels in Cord Blood of Term Low Birth Weight Neonates Requiring Delivery Room Resuscitation

2021 ◽  
pp. 097321792199140
Author(s):  
Rimjhim Sonowal ◽  
Anamika Jain ◽  
V. Bhargava ◽  
H.D. Khanna ◽  
Ashok Kumar
Keyword(s):  
Birth Weight ◽  
Low Birth Weight ◽  
Vitamin A ◽  
Cord Blood ◽  
Serum Levels ◽  
Study Groups ◽  
Delivery Room ◽  
Normal Birth Weight ◽  
Normal Birth ◽  
Major Congenital Malformations

Objective: The objective of this study was to evaluate the serum levels of various antioxidants, namely, vitamin A and E, superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) in the cord blood of term low birth weight (LBW) neonates who required delivery room resuscitation (DRR). Materials and Methods: This case control study included 37 term LBW neonates who needed DRR as cases and 44 term neonates as controls (15 term LBW and 29 term normal birth weight) who did not require resuscitation at birth. Neonates suffering from major congenital malformations, infection, or hemolytic disease were excluded. Standard methods were used to measure the levels of vitamin A, vitamin E, SOD, catalase, and GPx levels in the cord blood. Results: Vitamin A and E levels were significantly low in cases compared to term LBW controls as well as term normal birth weight controls. Levels of SOD, GPx, and catalase were comparable in different study groups. Conclusion: Our study shows that term LBW neonates requiring DRR had significantly low levels of vitamin A and E in their cord blood. This might compromise their ability to tolerate oxidative stress during DRR.

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