Pyridoxal-5-phosphate mitigates age-related metabolic imbalances in the rat heart through the HS/AKT/GSK3β signaling axis.

Pyridoxal-5-phosphate (PLP) enhances the synthesis of endogenous hydrogen sulfide, a potent regulator of cell metabolism. We used 24-month-old rats to investigate the PLP mitoprotective function in the aging heart. We demonstrated improvement of mitochondrial bioenergetic functions, inhibition of mPTP opening after PLP administration.

A multifactorial study of in situ antioxidant activity of modified GrO in myocardial reperfusion injury using the Langerdorff model.

Carbon nanomaterials possess antioxidant properties that can be applied in biomedicine and clinics for the development of new highly effective treatments against oxidative stress-induced diseases like ischemic heart disease. We previously reported the usage of graphene oxide (GrO) as a precursor for the elaboration of such prototypes. The promising findings led to the development of two new modifications of GrO: nitrogen-doped (N-GrO) and l-cysteine functionalized (S-GrO) derivatives as possible antioxidant agents in ischemia-reperfusion (I/R) conditions.

Glutathione Upregulates the Expression of K Channels and Vasorelaxation Responses and Inhibits mPTP Opening and Oxidative Stress in the Heart Mitochondria of Old Rats.

Background: In the present work, we investigated the effect of exogenous glutathione in old rats on the expression of ATP-sensitive potassium (K) channels, the mitochondrial permeability transition pore (mPTP) opening in the heart, and the vasorelaxation responses of isolated aortic rings to activation of K channels.

Methods: Experiments were performed on adult (6 months) and old (24 months) male Wistar rats, which were divided into three groups: adult, old, and glutathione-treated old rats. Glutathione was injected intraperitoneally at a dose of 52 mg/kg 1 hour before the studies.

Glutathione restores the mitochondrial redox status and improves the function of the cardiovascular system in old rats.

Aging is accompanied by cardiovascular disorders which is associated with an imbalance of pro- and antioxidant systems, the mitochondrial dysfunction, etc. Glutathione (GSH) plays a critical role in protecting cells from oxidative damage. The aim of the work was to study the effect of exogenous glutathione on the redox status of mitochondria, the content of HS and the function of the cardiovascular system in old rats.

Exercise restores endogenous H S synthesis and mitochondrial function in the heart of old rats.

Background: Ageing is accompanied by a decrease in endogenous hydrogen sulphide (H S) synthesis and the development of mitochondrial dysfunction. The aim of our work was to study the possible participation of exercise training-induced regulation of endogenous H S production in the restoration of mitochondrial function in old rats.

Materials And Methods: Male rats were divided into three groups: adult, old and exercise-trained old.

Graphene oxide nanoflakes prevent reperfusion injury of Langendorff isolated rat heart providing antioxidative activity in situ.

Carbon materials possess powerful antioxidant activity that might be promising for the development of new generation treatment of cardiovascular diseases, ischemic conditions, and reperfusion injury. The present study aimed to characterize the structure of nanosized graphene oxide (GrO) sample and evaluate the antioxidant efficacy of GrO models of oxidative stress widely used in pre-clinical studies. The structure and surface chemistry of the initial samples were analyzed LDS, RAMAN, LDI, TPD-MS, and FTIR methods.

Stimulation of mitochondrial hydrogen sulfide and glutathione production improves the Frank-Starling response of the rat heart via a nitric oxide-dependent pathway.

The Frank-Starling response of the heart is known to be mediated by nitric oxide (NO) signaling, which is regulated by reduced glutathione (GSH) and hydrogen sulfide (HS). We hypothesized that stimulation of endogenous HS or GSH synthesis would improve the Frank-Starling response. Wistar male rats were injected with propargylglycine (PAG; 11.

Induction of Glutathione Synthesis Provides Cardioprotection Regulating NO, AMPK and PPARa Signaling in Ischemic Rat Hearts.

Glutathione (GSH) is essential for antioxidant defence, and its depletion is associated with tissue damage during cardiac ischemia-reperfusion (I/R). GSH is synthesized by the glutamate-cysteine ligase enzyme (GCL) from L-cysteine, which alternatively might be used for hydrogen sulfide production by cystathionine-gamma-lyase (CSE). Here, we have investigated whether in vivo treatment with L-cysteine and an inhibitor of CSE,D,L-propargylglycine (PAG), can modulate cardiac glutathione and whether this treatment can influence heart resistance to I/R in a Langendorff isolated rat hearts model.