scholarly journals Short-Term Neonatal Oral Administration of Oleanolic Acid Protects against Fructose-Induced Oxidative Stress in the Skeletal Muscles of Suckling Rats

Molecules ◽  
2019 ◽  
Vol 24 (4) ◽  
pp. 661 ◽  
Author(s):  
Trevor Nyakudya ◽  
Simon Isaiah ◽  
Ademola Ayeleso ◽  
Ashwell Ndhlala ◽  
Emmanuel Mukwevho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastrointestinal Tract ◽  
Health Outcomes ◽  
Oleanolic Acid ◽  
Lipid Content ◽  
Skeletal Muscles ◽  
Neonatal Period ◽  
Short Term ◽  
Suckling Rats ◽  
Anti Oxidant

Nutritional manipulations in the neonatal period are associated with the development of negative or positive health outcomes later in life. Excessive fructose consumption has been attributed to the increase in the global prevalence of metabolic syndrome (MetS) and the development of oxidative stress. Oleanolic acid (OA) has anti-diabetic and anti-obesity effects. We investigated the protective potential of orally administering OA in the neonatal period, to prevent fructose-induced oxidative stress, adverse health outcomes and maturation of the gastrointestinal tract (GIT) in suckling rats. Seven-day old Sprague-Dawley rats (N = 30) were gavaged daily with 10 mL/kg of: distilled water (DW), oleanolic acid (OA; 60 mg/kg), high fructose solution (HF; 20% w/v), or OAHF for 7 days. On day 14, tissue samples were collected to determine clinical health profiles, hepatic lipid content, and activity of anti-oxidant enzymes. Furthermore, biomarkers of oxidative stress and anti-oxidant capacity in the skeletal muscles were assessed. The gastrointestinal tract (GIT) morphometry was measured. Rats in all groups grew over the 7-day treatment period. There were no significant differences in the terminal body masses, GIT morphometry, surrogate markers of general health, liver lipid content across all treatment groups (p < 0.05). Neonatal fructose administration decreased the activity of catalase, depleted GSH and increased lipid peroxidation. However, the level of GSH and catalase activity were improved by neonatal OA treatment. Short-term oral OA administration during the critical developmental period protects against fructose-induced oxidative stress without adverse effects on health outcomes associated with MetS or precocious development of the GIT in suckling male and female rats.

Pharmacological study on the possible involvement of a Nrf2 -Heme oxygenase pathways in anti-cataract activity of fisetin

2020 ◽  
Vol 10 (1) ◽  
pp. 14-19
Author(s):  
Krishna Reddy BV ◽  
Avinash Kumar Reddy G ◽  
Sujitha V ◽  
Manasa A
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Pharmacological Study ◽  
World Population ◽  
Central Feature ◽  
Beneficial Effects ◽  
Radical Production ◽  
Anti Oxidant ◽  
Diabetic Population ◽  
Oxidant Status

DM otherwise diabetes is now a days an epidemic with the percentage of patient population rising to almost 10% of the world population. Out of all the DM complications, cataract leads the way contributing to disabilities to about 60% of diabetic population. But the pathogenesis of DM cataract is still a half-understood area of medicine there by posing a problem in the therapy. The data that we have till now gives us enough evidence to advocate the oxidative stress has a major role for the pathogenesis of DM complications like DMnephropathy, DMneuropathy, and cardiac hypertrophy, which suggests the oxidative stress is a central feature of diabetes. In the current research, the pharmacological evaluation of Fisetin for its DM based anti-cataract property was performed. This research concentrates to estimate the possible involvement of Nrf-2 / heme oxygenase (HO)-pathway in the observed therapeutic effect, if any. The data obtained in this study also indicate that the observed beneficial effects mainly due to activation of Nrf2/HO-1 pathway. These effects probably result in increased tissue anti-oxidant status as well as decreased free radical production, which ultimately responsible for the observed beneficial effects of Fisetin against hyperglycemia-induced cataract.

scholarly journals Fighting Oxidative Stress with Sulfur: Hydrogen Sulfide in the Renal and Cardiovascular Systems

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 373
Author(s):  
Joshua J. Scammahorn ◽  
Isabel T. N. Nguyen ◽  
Eelke M. Bos ◽  
Harry Van Goor ◽  
Jaap A. Joles
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Redox Status ◽  
The Body ◽  
Therapeutic Interventions ◽  
Oxygen Species ◽  
Enzymatic Production ◽  
Age Related ◽  
Anti Oxidant ◽  
Enzymatic Pathways

Hydrogen sulfide (H2S) is an essential gaseous signaling molecule. Research on its role in physiological and pathophysiological processes has greatly expanded. Endogenous enzymatic production through the transsulfuration and cysteine catabolism pathways can occur in the kidneys and blood vessels. Furthermore, non-enzymatic pathways are present throughout the body. In the renal and cardiovascular system, H2S plays an important role in maintaining the redox status at safe levels by promoting scavenging of reactive oxygen species (ROS). H2S also modifies cysteine residues on key signaling molecules such as keap1/Nrf2, NFκB, and HIF-1α, thereby promoting anti-oxidant mechanisms. Depletion of H2S is implicated in many age-related and cardiorenal diseases, all having oxidative stress as a major contributor. Current research suggests potential for H2S-based therapies, however, therapeutic interventions have been limited to studies in animal models. Beyond H2S use as direct treatment, it could improve procedures such as transplantation, stem cell therapy, and the safety and efficacy of drugs including NSAIDs and ACE inhibitors. All in all, H2S is a prime subject for further research with potential for clinical use.

scholarly journals Oxidative Stress, Glutathione Metabolism, and Liver Regeneration Pathways Are Activated in Hereditary Tyrosinemia Type 1 Mice upon Short-Term Nitisinone Discontinuation

Genes ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 3
Author(s):  
Haaike Colemonts-Vroninks ◽  
Jessie Neuckermans ◽  
Lionel Marcelis ◽  
Paul Claes ◽  
Steven Branson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Liver Regeneration ◽  
The Body ◽  
Glutathione Metabolism ◽  
Short Term ◽  
Therapeutic Regime ◽  
Tyrosinemia Type 1 ◽  
Hereditary Tyrosinemia

Hereditary tyrosinemia type 1 (HT1) is an inherited condition in which the body is unable to break down the amino acid tyrosine due to mutations in the fumarylacetoacetate hydrolase (FAH) gene, coding for the final enzyme of the tyrosine degradation pathway. As a consequence, HT1 patients accumulate toxic tyrosine derivatives causing severe liver damage. Since its introduction, the drug nitisinone (NTBC) has offered a life-saving treatment that inhibits the upstream enzyme 4-hydroxyphenylpyruvate dioxygenase (HPD), thereby preventing production of downstream toxic metabolites. However, HT1 patients under NTBC therapy remain unable to degrade tyrosine. To control the disease and side-effects of the drug, HT1 patients need to take NTBC as an adjunct to a lifelong tyrosine and phenylalanine restricted diet. As a consequence of this strict therapeutic regime, drug compliance issues can arise with significant influence on patient health. In this study, we investigated the molecular impact of short-term NTBC therapy discontinuation on liver tissue of Fah-deficient mice. We found that after seven days of NTBC withdrawal, molecular pathways related to oxidative stress, glutathione metabolism, and liver regeneration were mostly affected. More specifically, NRF2-mediated oxidative stress response and several toxicological gene classes related to reactive oxygen species metabolism were significantly modulated. We observed that the expression of several key glutathione metabolism related genes including Slc7a11 and Ggt1 was highly increased after short-term NTBC therapy deprivation. This stress response was associated with the transcriptional activation of several markers of liver progenitor cells including Atf3, Cyr61, Ddr1, Epcam, Elovl7, and Glis3, indicating a concreted activation of liver regeneration early after NTBC withdrawal.

Effect of Intraduodenal Starch Infusion on Net Portal Absorption of Amino Acids in Growing steers Fed Lucerne

1994 ◽  
Vol 1994 ◽  
pp. 28-28
Author(s):  
C.J. Seal ◽  
D.S. Parker ◽  
J.C. MacRae ◽  
G.E. Lobley
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Gastrointestinal Tract ◽  
Protein Turnover ◽  
Portal Blood ◽  
Intestinal Lumen ◽  
Short Term ◽  
Net Uptake ◽  
Amino Acid Requirements ◽  
Glucose Availability

Amino acid requirements for energy metabolism and protein turnover within the gastrointestinal tract are substantial and may be met from luminal and arterial pools of amino acids. Several studies have demonstrated that the quantity of amino acids appearing in the portal blood does not balance apparent disappearance from the intestinal lumen and that changing diet or the availability of energy-yielding substrates to the gut tissues may influence the uptake of amino acids into the portal blood (Seal & Reynolds, 1993). For example, increased net absorption of amino acids was observed in animals receiving exogenous intraruminal propionate (Seal & Parker, 1991) and this was accompanied by changes in glucose utilisation by the gut tissues. In contrast, there was no apparent change in net uptake of [l-13C]-leucine into the portal vein of sheep receiving short term intraduodenal infusions of glucose (Piccioli Cappelli et al, 1993). This experiment was designed to further investigate the effects on amino acid absorption of changing glucose availability to the gut with short term (seven hours) or prolonged (three days) exposure to starch infused directly into the duodenum.

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