scholarly journals The 1-Week and 8-Month Effects of a Ketogenic Diet or Ketone Salt Supplementation on Multi-Organ Markers of Oxidative Stress and Mitochondrial Function in Rats

Nutrients ◽  
2017 ◽  
Vol 9 (9) ◽  
pp. 1019 ◽  
Author(s):  
Wesley Kephart ◽  
Petey Mumford ◽  
Xuansong Mao ◽  
Matthew Romero ◽  
Hayden Hyatt ◽  
...  
Life Sciences ◽  
2021 ◽  
pp. 120227
Author(s):  
Pedro Rojas-Morales ◽  
Juan Carlos León-Contreras ◽  
Mónica Sánchez-Tapia ◽  
Alejandro Silva-Palacios ◽  
Agustina Cano-Martínez ◽  
...  

2021 ◽  
Vol 22 (7) ◽  
pp. 3498
Author(s):  
Guglielmina Chimienti ◽  
Antonella Orlando ◽  
Angela Maria Serena Lezza ◽  
Benedetta D’Attoma ◽  
Maria Notarnicola ◽  
...  

Functional alterations in irritable bowel syndrome have been associated with defects in bioenergetics and the mitochondrial network. Effects of high fat, adequate-protein, low carbohydrate ketogenic diet (KD) involve oxidative stress, inflammation, mitochondrial function, and biogenesis. The aim was to evaluate the KD efficacy in reducing the effects of stress on gut mitochondria. Newborn Wistar rats were exposed to maternal deprivation to induce IBS in adulthood. Intestinal inflammation (COX-2 and TRL-4); cellular redox status (SOD 1, SOD 2, PrxIII, mtDNA oxidatively modified purines); mitochondrial biogenesis (PPAR-γ, PGC-1α, COX-4, mtDNA content); and autophagy (Beclin-1, LC3 II) were evaluated in the colon of exposed rats fed with KD (IBD-KD) or standard diet (IBS-Std), and in unexposed controls (Ctrl). IBS-Std rats showed dysfunctional mitochondrial biogenesis (PPAR-γ, PGC-1α, COX-4, and mtDNA contents lower than in Ctrl) associated with inflammation and increased oxidative stress (higher levels of COX-2 and TLR-4, SOD 1, SOD 2, PrxIII, and oxidatively modified purines than in Ctrl). Loss of autophagy efficacy appeared from reduced levels of Beclin-1 and LC3 II. Feeding of animals with KD elicited compensatory mechanisms able to reduce inflammation, oxidative stress, restore mitochondrial function, and baseline autophagy, possibly via the upregulation of the PPAR-γ/PGC-1α axis.


Drug Research ◽  
2019 ◽  
Vol 70 (01) ◽  
pp. 49-56 ◽  
Author(s):  
Mohammad Mehdi Ommati ◽  
Omid Farshad ◽  
Vahid Ghanbarinejad ◽  
Hamid Reza Mohammadi ◽  
Mousavi Khadijeh ◽  
...  

Abstract Background Ifosfamide (IFO) is an alkylating agent administered against different types of malignancies. Several cases of renal injury and serum electrolytes disturbances have been reported in IFO-treated patients. Oxidative stress and mitochondrial dysfunction are suspected of being involved in the mechanism of IFO nephrotoxicity. Carnosine is a dipeptide which its antioxidant and mitochondria protecting properties have been mentioned in different experimental models. The current study aimed to evaluate the nephroprotective properties of carnosine against IFO-induced renal injury. Methods Rats were treated with IFO (50 mg/kg, i.p) alone or in combination with carnosine. Serum and urine biomarkers of renal injury in addition to kidney markers of oxidative stress were evaluated. Moreover, kidney mitochondria were isolated, and some mitochondrial indices were assessed. Results Elevated serum creatinine and BUN, hypokalemia, and hypophosphatemia, in addition, to an increase in urine glucose, protein, γ-GT, and alkaline phosphatase (ALP), were evident in IFO-treated animals. IFO also caused an increase in kidney reactive oxygen species (ROS) and lipid peroxidation (LPO). Renal GSH levels and antioxidant capacity were also depleted with IFO therapy. Mitochondrial dehydrogenase activity, GSH level, membrane potential, and ATP content were decreased while mitochondrial LPO and permeabilization were increased in IFO group. Carnosine (250 and 500 mg/kg, i.p) mitigated IFO-induced oxidative stress and mitochondrial impairment in renal tissue. Conclusion Our data suggest mitochondrial dysfunction and oxidative stress as fundamental mechanisms of renal injury induced by IFO. On the other hand, carnosine supplementation protected kidneys against IFO-induced injury through regulating mitochondrial function and mitigating oxidative stress.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Alexandra Gaál Kovalčíková ◽  
Ľubica Tichá ◽  
Katarína Šebeková ◽  
Peter Celec ◽  
Alžbeta Čagalová ◽  
...  

Abstract Background Anorexia nervosa (AN) is a serious psychosomatic disorder with unclear pathomechanisms. Metabolic dysregulation is associated with disruption of redox homeostasis that might play a pivotal role in the development of AN. The aim of our study was to assess oxidative status and carbonyl stress in plasma, urine and saliva of patients with AN and healthy controls. Methods Plasma, spot urine, and saliva were collected from 111 girls with AN (aged from 10 to 18 years) and from 29 age-matched controls. Markers of oxidative stress and antioxidant status were measured using spectrophotometric and fluorometric methods. Results Plasma advanced oxidation protein products (AOPP) and advanced glycation end products (AGEs) were significantly higher in patients with AN than in healthy controls (by 96, and 82%, respectively). Accordingly, urinary concentrations of AOPP and fructosamines and salivary concentrations of AGEs were higher in girls with AN compared with controls (by 250, and 41% in urine; by 92% in saliva, respectively). Concentrations of thiobarbituric acid reactive substances (TBARS) in saliva were 3-times higher in the patients with AN than in the controls. Overall antioxidants were lower in plasma of girls with AN compared to the controls, as shown by total antioxidant capacity and ratio of reduced and oxidized glutathione (by 43, and 31%, respectively). Conclusions This is the first study assessing wide range of markers of oxidative status in plasma, urine and saliva of the patients with AN. We showed that both, higher levels of markers of oxidative stress and lower antioxidants play a role in redox disruption. Restoration of redox homeostasis might be of the clinical relevance


Author(s):  
Sicong Yu ◽  
Lepeng Gao ◽  
Yang Song ◽  
Xin Ma ◽  
Shuang Liang ◽  
...  

Abstract Mitochondria play an important role in controlling oocyte developmental competence. Our previous studies showed that glycine can regulate mitochondrial function and improve oocyte maturation in vitro. However, the mechanisms by which glycine affects mitochondrial function during oocyte maturation in vitro have not been fully investigated. In this study, we induced a mitochondrial damage model in oocytes with the Bcl-2-specific antagonist ABT-199. We investigated whether glycine could reverse the mitochondrial dysfunction induced by ABT-199 exposure and whether it is related to calcium regulation. Our results showed that ABT-199 inhibited cumulus expansion, decreased the oocyte maturation rate and the intracellular glutathione (GSH) level, caused mitochondrial dysfunction, induced oxidative stress, which was confirmed by decreased mitochondrial membrane potential (Δ⍦m) and the expression of mitochondrial function-related genes (PGC-1α), and increased reactive oxygen species (ROS) levels and the expression of apoptosis-associated genes (Bax, caspase-3, CytC). More importantly, ABT-199-treated oocytes showed an increase in the intracellular free calcium concentration ([Ca 2+]i) and had impaired cortical type 1 inositol 1,4,5-trisphosphate receptors (IP3R1) distribution. Nevertheless, treatment with glycine significantly ameliorated mitochondrial dysfunction, oxidative stress and apoptosis, glycine also regulated [Ca 2+]i levels and IP3R1 cellular distribution, which further protects oocyte maturation in ABT-199-induced porcine oocytes. Taken together, our results indicate that glycine has a protective action against ABT-199-induced mitochondrial dysfunction in porcine oocytes.


Author(s):  
Juana Rosado-Pérez ◽  
Osvaldo D. Castelán-Martínez ◽  
Abril J. Mújica-Calderón ◽  
Martha A. Sánchez-Rodríguez ◽  
Víctor Manuel Mendoza-Núñez

Background: This study aimed to synthesize the evidence of the effect of practicing Tai Chi on oxidative stress markers (OxSM). Methods: This systematic review and meta-analysis was conducting using the MEDLINE, Cochrane Library, ScienceDirect, Scopus, Epistemonikos, Lilacs, and Ovid databases to identify randomized (RCT) and non-randomized (NRCT) clinical trials that evaluated the Tai Chi effect on OxSM compared to sedentary behavior, walking or yoga. Pooled mean differences (MDs) with 95% confidence intervals (95%CI) were estimated using the inverse variance method to determine the effect of Tai Chi on OxSM. PROSPERO register: CRD42019138362. Results: Five RCT and five NRCT were included. Compared to sedentary behavior, regular Tai Chi practice increases the levels of the enzymes superoxide dismutase (MD = 34.97 U/mL, (95%CI, 9.45 to 60.48), 344 participants) and catalase (MD = 15.63 U/mL, (95%CI, 4.05 to 27.22), 110 participants), as well as reducing the levels of lipoperoxides (MD = −0.02 µmol/L, (95%CI, −0.04 to −0.00), 234 participants). For comparisons with walking or yoga, only one study per activity was identified comparing the effect on OxSM. Conclusions: Regular Tai Chi practice increases the levels of superoxide dismutase and catalase, as well as reducing the levels of lipoperoxides. More studies are necessary to determine the effect of Tai Chi on OxSM when compared to other physical activities.


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