The physical exercise-induced oxidative/inflammatory response in peripheral blood mononuclear cells: Signaling cellular energetic stress situations.

Peripheral blood mononuclear cells (PBMCs) are a variety of specialized immune cells produced in the bone marrow from hematopoietic stem cells (HSCs) that work together to protect our bodies from harmful pathogens. From a metabolic point of view, these cells can serve as sentinel tissue source for distinguishing multiple types of whole-body physiological perturbations. The significant interaction of PBMCs with systemic physiology makes these cells an attractive target for several interventions such as physical exercise.

Guanosine protects against behavioural and mitochondrial bioenergetic alterations after mild traumatic brain injury.

Traumatic brain injury (TBI) constitutes a heterogeneous cerebral insult induced by traumatic biomechanical forces. Mitochondria play a critical role in brain bioenergetics, and TBI induces several consequences related with oxidative stress and excitotoxicity clearly demonstrated in different experimental model involving TBI. Mitochondrial bioenergetics alterations can present several targets for therapeutics which could help reduce secondary brain lesions such as neuropsychiatric problems, including memory loss and motor impairment.

Diclofenac attenuates inflammation through TLR4 pathway and improves exercise performance after exhaustive swimming.

Background: The use of NSAIDs has become a common practice to counteract the pro-inflammatory acute effects of exercise, in order to improve sports performance. The liver, due to its central role in energy metabolism, may be involved primarily in the process of ROS generation and consequently inflammation after exhaustive exercise.

Objective: To analyze the influence of diclofenac on the liver TLR4 pathway and time to exhaustion in rats submitted to repeated exhaustive swimming.

Guanosine protects against Ca-induced mitochondrial dysfunction in rats.

Mitochondria play an important role in cell life and in the regulation of cell death. In addition, mitochondrial dysfunction contributes to a wide range of neuropathologies. The nucleoside Guanosine (GUO) is an endogenous molecule, presenting antioxidant properties, possibly due to its direct scavenging ability and/or from its capacity to activate the antioxidant defense system.

Antioxidant protection by β-selenoamines against thioacetamide-induced oxidative stress and hepatotoxicity in mice.

Thioacetamide (TAA) is a hepatotoxin that rapidly triggers the necrotic process and oxidative stress in the liver. Nevertheless, organic selenium compounds, such as β-selenoamines, can be used as pharmacological agents to diminish the oxidative damage. Thus, the aim of this study was to investigate the protective effect of the antioxidant β-selenoamines on TAA-induced oxidative stress in mice.