The aging process is a complex phenomenon that leads the body to several changes, affecting its integrity and resulting in chronic pathologies, which compromises health and quality of life of elderly people. Animals supplemented with fructose have been used as an experimental model for induction of insulin resistance. The objective of this study was to evaluate the metabolic effects and the levels of oxidative/nitrosative stress in the kidney of senescent rats with a high fructose intake. The animals were allocated into 4 groups: young control (Y), aged control (A), young fructose (YF) and aged fructose (AF). Groups Y and A received water and groups YF and AF received fructose (100g/L) in the water, both ad libitum. After 12weeks of high fructose intake, the animals were sacrificed to collect their kidneys, blood and the thoracic aorta. The results are presented as mean±SE, analyzed by the One-Way ANOVA test with Newman-Keuls post-test; significant at p<0.05. The fructose overload caused metabolic dysfunctions and insulin resistance, confirming the efficacy of the chosen model. In this study, we observed a body weight gain in the studied groups (except in the elderly fructose group), and an increase in general caloric intake, diuresis and adipose tissue; insulin resistance, increased fasting glucose, triglycerides and cholesterol in the fructose groups. We also found a loss of renal function, increased oxidative/nitrosative stress and inflammation, and a reduction of antioxidants and a lower vasodepressor response in the studied groups, especially those who consumed fructose. In summary, our data showed that aging or high fructose intake contributed to the increase of oxidative/nitrosative stress in animals, demonstrating that at the dose and the period of fructose treatment utilized in this study, fructose was not able to aggravate several aspects which were already altered by aging. We believe that the high fructose intake simulates most of the effects of aging, and this understanding would be useful to prevent or minimize many of the alterations caused by this condition.
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http://dx.doi.org/10.1016/j.exger.2017.09.011 | DOI Listing |
Aquat Toxicol
January 2025
Department of Marine Biology, Institute for Biological Sciences, University of Rostock, Rostock, Germany; Department of Maritime Systems, Interdisciplinary Faculty, University of Rostock, Rostock, Germany. Electronic address:
Lipid-lowering drugs such as gemfibrozil (GFB) are widely used and highly biologically active, contributing to their persistence in wastewater and subsequent release into aquatic ecosystems. However, the potential impacts and toxic mechanisms of these emerging pollutants on non-target marine organisms, particularly keystone bivalves like Mytilus edulis, remain poorly understood. To address this knowledge gap, we investigated the effects of environmentally relevant concentrations of GFB (25 µg l) on oxidative, nitrosative, and dicarbonyl stress in M.
View Article and Find Full Text PDFArch Physiol Biochem
January 2025
Laboratório de Fisiologia Cardiovascular, Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
This study explored the effects of melatonin on cardiac and vascular function, and redox homeostasis in model PAH. Male Wistar rats were divided into: control (CTR), monocrotaline [MCT (60 mg/kg, single dose i.p)], monocrotaline + sildenafil [MCT + SIL (50 mg/kg/day)], and monocrotaline + melatonin [MCT + MEL (10 mg/kg/day)].
View Article and Find Full Text PDFEnviron Toxicol
December 2024
Department of Biological Sciences (Regulatory Toxicology), National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, Telangana, India.
AMP-activated protein kinase (AMPK) is the master regulator of cellular energy which gets activated during energy stress and restores tissue homeostasis. AMPK is widely expressed in the pancreas and is involved in protein synthesis. In cerulein-induced acute pancreatitis (AP), diminished AMPK activity in the pancreatic tissue may be associated with pancreatic inflammation and oxidative stress.
View Article and Find Full Text PDFFront Cell Dev Biol
December 2024
Department of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Changes to the composition of the microbiome in neoplasia, is termed oncobiosis, may affect tumor behavior through the changes to the secretion of bacterial metabolites. In this study we show, that ursodeoxycholic acid (UDCA), a bacterial metabolite, has cytostatic properties in pancreatic adenocarcinoma cell (PDAC) models. UDCA in concentrations corresponding to the human serum reference range suppressed PDAC cell proliferation.
View Article and Find Full Text PDFTalanta
December 2024
School of Water Conservancy and Environment, University of Jinan, Jinan, 250022, China. Electronic address:
Drug-induced liver injury (DILI) is a crucial factor that poses a significant threat to human health. DILI process leads to the changes of reactive oxygen species and reactive nitrogen species content in cells, which leads to oxidative and nitrosative stress in cells. However, the high reactivity of hypochlorous acid (HOCl) and peroxynitrite (ONOO⁻), combined with a lack of in situ imaging techniques, has hindered a detailed understanding of their roles in DILI.
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