Green synthesis of gold nanoparticles modulates lipopolysaccharide-induced lung inflammation in Wistar rats.

This study aimed to investigate the effect of intranasal treatment of gold nanoparticles (GNPs) and Curcumin (Cur) on the lipopolysaccharide (LPS)-induced acute pulmonary inflammatory response. A single intraperitoneal injection of LPS (0.5 mg/Kg) was performed, and the animals in the Sham group were injected with 0.9% saline. Treatment was daily intranasally with GNPs (2.5 mg/L), Cur (10 mg/kg) and GNP-Cur started 12 h after LPS administration and ended on the seventh day. The results show that the treatment performed with GNP-Cur was the most effective to attenuate the action of pro-inflammatory cytokines, and a lower leukocyte count in the bronchoalveolar lavage, in addition to positively regulating anti-inflammatory cytokines in relation to other groups. As a result, it promoted an oxirreductive balanced environment in the lung tissue, providing a histological outcome with a reduction in inflammatory cells and greater alveolar area. The group treated with GNPs-Cur was superior to the other groups, with better anti-inflammatory activity and reduced oxidative stress, resulting in less morphological damage to lung tissue. In conclusion, the use of reduced GNPs with curcumin demonstrates promising effects in the control of the acute inflammatory response, helping to protect the lung tissue at the biochemical and morphological levels.

Acute effects of intracerebroventricular administration of α-ketoisocaproic acid in young rats on inflammatory parameters.

Maple Syrup Urine Disease (MSUD) is an autosomal recessive inborn error of metabolism (IEM), responsible for the accumulation of the branched-chain amino acids (BCAA) leucine, isoleucine, and valine, in addition to their α-keto acids α-ketoisocaproic acid (KIC), α-keto-ß-methylvaleric acid (KMV), and α-ketoisovaleric acid (KIV) in the plasma and urine of patients. This process occurs due to a partial or total blockage of the dehydrogenase enzyme activity of branched-chain α-keto acids. Oxidative stress and inflammation are conditions commonly observed on IEM, and the inflammatory response may play an essential role in the pathophysiology of MSUD. We aimed to investigate the acute effect of intracerebroventricular (ICV) administration of KIC on inflammatory parameters in young Wistar rats. For this, sixteen 30-day-old male Wistar rats receive ICV microinjection with 8 µmol KIC. Sixty minutes later, the animals were euthanized, and the cerebral cortex, hippocampus, and striatum structures were collected to assess the levels of pro-inflammatory cytokines (INF-γ; TNF-α, IL-1ß). The acute ICV administration of KIC increased INF-γ levels in the cerebral cortex and reduced the levels of INF-γ and TNF-α in the hippocampus. There was no difference in IL-1ß levels. KIC was related to changes in the levels of pro-inflammatory cytokines in the brain of rats. However, the inflammatory mechanisms involved in MSUD are poorly understood. Thus, studies that aim to unravel the neuroinflammation in this pathology are essential to understand the pathophysiology of this IEM.

Effects of diet-induced hypercholesterolemia and gold nanoparticles treatment on peripheral tissues.

Cholesterol is a lipid molecule of great biological importance to animal cells. Dysregulation of cholesterol metabolism leads to raised blood total cholesterol levels, a clinical condition called hypercholesterolemia. Evidence has shown that hypercholesterolemia is associated with the development of liver and heart disease. One of the mechanisms underlying heart and liver alterations induced by hypercholesterolemia is oxidative stress. In this regard, in several experimental studies, gold nanoparticles (AuNP) displayed antioxidant properties. We hypothesized that hypercholesterolemia causes redox system imbalance in the liver and cardiac tissues, and AuNP treatment could ameliorate it. Young adult male Swiss mice fed a regular rodent diet or a high cholesterol diet for eight weeks and concomitantly treated with AuNP (2.5 µg/kg) or vehicle by oral gavage. Hypercholesterolemia increased the nitrite concentration and glutathione (GSH) levels and decreased the liver's superoxide dismutase (SOD) activity. Also, hypercholesterolemia significantly enhanced the reactive oxygen species (ROS) and GSH levels in cardiac tissue. Notably, AuNP promoted the redox system homeostasis, increasing the SOD activity in hepatic tissue and reducing ROS levels in cardiac tissue. Overall, our data showed that hypercholesterolemia triggered oxidative stress in mice's liver and heart, which was partially prevented by AuNP treatment.

The Use of Metallic Nanoparticles in Wound Healing: New Perspectives.

Chronic wounds represent a challenge for the health area, as they directly impact patients' quality of life and represent a threat to public health and the global economy due to their high cost of treatment. Alternative strategies must be developed for cost-effective and targeted treatment. In this scenario, the emerging field of nanobiotechnology may provide an alternative platform to develop new therapeutic agents for the chronic wound healing process. This manuscript aims to demonstrate that the application of metallic nanoparticles (gold, silver, copper, and zinc oxide) opened a new chapter in the treatment of wounds, as they have different properties such as drug delivery, antimicrobial activity, and healing acceleration. Furthermore, metallic nanoparticles (NPs) produced through green synthesis ensure less toxicity in biological tissues, and greater safety of applicability, other than adding the effects of NPs with those of extracts.

Gold Nanoparticle-Based Therapy for Muscle Inflammation and Oxidative Stress.

Proinflammatory cytokines and reactive oxygen species are released after muscle damage, and although they are necessary for the muscle regeneration process, an excess of these substances leads to the destruction of biomolecules and impairment of the repair system. Several drugs have emerged in recent years to control the muscle inflammatory response, and studies have shown that gold nanoparticles (AuNPs) have anti-inflammatory and antioxidant properties. This review reveals the effects of AuNPs on the inflammatory and redox mechanisms of muscles. We assessed the results of several studies published in different journals over the last 20 years, with a focus on the effects of AuNPs on possible aspects of muscle regeneration or recovery, namely, inflammatory processes and redox system mechanisms. A systematic database search was conducted using PubMed, Medline, Bireme, Web of Science, and Google Scholar to identify peer-reviewed studies from the 2000s. Combinations of keywords related to muscle damage, regeneration or repair, AuNPs, oxidative stress, and antioxidants were used in the search. This review did not address other variables, such as specific diseases or other biological effects; however, these variables should be considered for a complete understanding of the effects of AuNPs on skeletal muscles.

Effect of taurine associated gold nanoparticles on oxidative stress in muscle of mice exposed to overuse model.

Muscle overuse and its consequent muscle damage has no cure. Therefore, the present study aimed to investigate the regulatory role of tau-AuNPs on muscle recovery of muscle overuse model. The animals (Male Swiss mice) were randomly divided into four groups: Control (Ctr; n=6); tau-AuNPs (n=6); overuse (n=6); and overuse plus tau-AuNPs (n=6). Exercise sessions were performed for 21 consecutive days, and one exercise model was applied daily in the following sequence: low intensity, moderate intensity, and high intensity. The mice were then sacrificed. The quadriceps muscles were surgically removed for subsequent biochemical analysis (oxidative stress parameters, DNA damage markers and muscle differentiation protein). The overuse group significantly increased the oxidative stress parameters and DNA damage markers, whereas tau-AuNPs significantly decreased the oxidative stress parameters in the overuse animal model. However, there were no significant differences observed between overuse group and overuse plus tau-AuNPs administrated group in relation to DNA damage markers including DNA damage frequency and index levels when compared to control and tau-AuNPs groups. Muscle differentiation protein Myf-5 was increased in the overuse plus tau-AuNPs administration group when compared to control group. In conclusion, tau-AuNPs had significant effect on reducing oxidative stress parameters and increasing myogenic regulatory protein Myf-5 in the overuse group. However, it did not have significant effect on reducing DNA damage.

Neuroinflammatory Regulation of Gold Nanoparticles Conjugated to Ethylene Dicysteine Diethyl Ester in Experimental Autoimmune Encephalomyelitis.

Multiple sclerosis (MS) is a demyelinating chronic autoimmune inflammatory disease of the central nervous system (CNS). A large amount of proinflammatory cytokines is released in the CNS from the self-reactive T cells infiltrate, leading to the destruction of the myelin sheath and contributing to the development of MS. Several drugs have emerged in recent years to treat MS, and studies have shown that gold nanoparticles (GNPs) have anti-inflammatory properties in autoimmune diseases. Thus, the effects of GNP conjugation to ethylene dicysteine diethyl ester (ECD) were evaluated in C57BL/6 female mice exposed to experimental MS. Animals were exposed to experimental autoimmune encephalitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG35-55) in complete Freund's adjuvant supplemented with Mycobacterium tuberculosis. The clinical and cerebral effects of the different doses of ECD-GNPs (0.3, 0.6, and 1.0 mg/kg) were first studied, and the results showed that the group treated with 0.6 mg/kg ECD-GNPs improved clinical symptoms, inflammatory infiltrate, and myelin integrity. In the following step, GNPs and ECD-GNPs (0.6 mg/kg) showed improvements in the clinical signs of the disease. Moreover, there was a reduction in the levels of proinflammatory cytokines in both groups compared to EAE, and only the isolated use of GNPs increased IL-4 expression. Both NF-κB and TGFß immunoexpression were significantly reduced following EAE + GNPs and EAE + ECD-GNPs treatment. In conclusion, GNPs and ECD-GNPs at 0.6 mg/kg attenuate the neurological signs of EAE likely due to inhibition of neuroinflammation induced by EAE.

Physical Exercise-Mediated Changes in Redox Profile Contribute to Muscle Remodeling After Passive Hand-Rolled Cornhusk Cigarette Smoke Exposure.

Consumption of non-traditional cigarettes has increased considerably worldwide, and they can induce skeletal muscle dysfunction. Physical exercise has been demonstrated to be important for prevention and treatment of smoking-related diseases. Therfore, the aim of this study was to investigate the effects of combined physical exercise (aerobic plus resistance exercise) on muscle histoarchitecture and oxidative stress in the animals exposed chronically to smoke from hand-rolled cornhusk cigarette (HRCC). Male Swiss mice were exposed to ambient air or passively to the smoke of 12 cigarettes over three daily sessions (four cigarettes per session) for 30 consecutive days with or without combined physical training. 48 h after the last training session, total leukocyte count was measured in bronchoalveolar lavage fluid (BALF), and the quadriceps were removed for histological/immunohistochemical analysis and measurement of oxidative stress parameters. The effects of HRCC on the number of leukocytes in BALF, muscle fiber diameter, central nuclei, and nuclear factor kappa B (NF-κB) were reverted after combined physical training. In addition, increased myogenic factor 5, tumor necrosis factor alpha (TNFα), reduced transforming growth factor beta (TGF-ß), and nitrate levels were observed after physical training. However, the reduction in superoxide dismutase and glutathione/glutathione oxidized ratio induced by HRCC was not affected by the training program. These results suggest the important changes in the skeletal muscle brought about by HRCC-induced alteration in the muscle redox profile. In addition, combined physical exercise contributes to remodeling without disrupting muscle morphology.

Improvement in muscular strength and aerobic capacities in elderly people occurs independently of physical training type or exercise model.

OBJECTIVES: Progressive decline of physiological processes with aging is normal. Aging is also associated with decreased functional capacity and onset of many diseases. This study evaluated the changes in physical fitness (PF), body composition (BC), and lipid profile (LP) in elderly men completing different training protocols. METHODS: Fifty-five men (age 60-80 years) were randomized into the following groups: without training, aerobic training on dry land, combined training on dry land, and combined training in water. Training was conducted for 8 weeks, and PF, LP, and BC were assessed at the beginning and end of the intervention. RESULTS: Significant improvements were observed in all parameters; however, combined programs on land or in water were more effective at improving strength and aerobic fitness. Combined exercise produced greater effects on BC and LP and some muscle fitness parameters; however, improvements in muscular and aerobic capacities occurred independently of exercise type or model. CONCLUSION: These results indicate that the effects of training occur regardless of training type or model, and are directly associated with training periodization, adherence, and regularity.

Improvement in muscular strength and aerobic capacities in elderly people occurs independently of physical training type or exercise model

OBJECTIVES: Progressive decline of physiological processes with aging is normal. Aging is also associated with decreased functional capacity and onset of many diseases. This study evaluated the changes in physical fitness (PF), body composition (BC), and lipid profile (LP) in elderly men completing different training protocols. METHODS: Fifty-five men (age 60-80 years) were randomized into the following groups: without training, aerobic training on dry land, combined training on dry land, and combined training in water. Training was conducted for 8 weeks, and PF, LP, and BC were assessed at the beginning and end of the intervention. RESULTS: Significant improvements were observed in all parameters; however, combined programs on land or in water were more effective at improving strength and aerobic fitness. Combined exercise produced greater effects on BC and LP and some muscle fitness parameters; however, improvements in muscular and aerobic capacities occurred independently of exercise type or model. CONCLUSION: These results indicate that the effects of training occur regardless of training type or model, and are directly associated with training periodization, adherence, and regularity.

Physical Exercise Attenuates Experimental Autoimmune Encephalomyelitis by Inhibiting Peripheral Immune Response and Blood-Brain Barrier Disruption.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) caused by demyelination, immune cell infiltration, and axonal damage. Herein, we sought to investigate the influence of physical exercise on mice experimental autoimmune encephalomyelitis (EAE), a reported MS model. Data show that both strength and endurance training protocols consistently prevented clinical signs of EAE and decreased oxidative stress, an effect which was likely due to improving genomic antioxidant defense-nuclear factor erythroid 2-related factor (Nrf2)/antioxidant response elements (ARE) pathway-in the CNS. In addition, physical exercise inhibited the production of pro-inflammatory cytokines interferon (IFN)-γ, interleukin (IL)-17, and IL-1ß in the spinal cord of mice with EAE. Of note, spleen cells obtained from strength training group incubated with MOG35-55 showed a significant upregulation of CD25 and IL-10 levels, with a decrease of IL-6, MCP-1, and tumor necrosis factor (TNF)-α production, mainly, during acute and chronic phase of EAE. Moreover, these immunomodulatory effects of exercise were associated with reduced expression of adhesion molecules, especially of platelet and endothelial cell adhesion molecule 1 (PECAM-1). Finally, physical exercise also restored the expression of tight junctions in spinal cord. Together, these results demonstrate that mild/moderate physical exercise, when performed regularly in mice, consistently attenuates the progression and pathological hallmarks of EAE, thereby representing an important non-pharmacological intervention for the improvement of immune-mediated diseases such as MS. Graphical Abstract Schematic diagram illustrating the beneficial effects of physical exercise during experimental model of MS. Physical exercise, especially strength (ST) and endurance (ET) training protocols, inhibits the development and progression of disease, measured by the mean maximal clinical score (1.5 and 1.0, respectively), with inhibition of 30 % and 50 %, respectively, based on the AUC, compared with EAEuntreated group. In addition, ST and ET decreased oxidative stress, possibly, through genomic antioxidant defense, Nrf2-Keap1 signaling pathway, in the CNS. Physical exercise inhibited the production of inflammatory cytokines, such as IFN-γ, IL-17 and IL-1ß in the spinal cord after EAE induction, as well as spleen cells obtained from ST group showed a significant upregulation of regulatory T cell markers, such as CD25 and IL-10 levels, and blocked IL-6, MCP-1 and TNF-α production, mainly, during acute and chronic phase of EAE. Finally, these immunomodulatory effects of exercise were associated with inhibition of adhesion molecules and reestablishment of tight junctions expression in spinal cord tissue, thereby limiting BBB permeability and transmigration of autoreactive T cells to the CNS. NO, nitric oxide; GPx, glutathione peroxidase, GSH, glutathione; Nrf2, nuclear factor (erythroid-derived 2)-like 2; CNS, central nervous system; BBB, blood-brain barrier; IFN-g, interferon-gamma; IL-17, interleukin 17; IL-1b, interleukin-1beta.

Effect of Low-Power Laser (LPL) and Light-Emitting Diode (LED) on Inflammatory Response in Burn Wound Healing.

The aim of the study was to investigate the biochemical and molecular changes in the process of epidermal healing of burn injuries after therapeutic treatment with low-power laser (LPL) and light-emitting diode (LED). Rats were divided into six groups: skin without injury (Sham), burn wounds (BWs), BW + 660-nm LPL, BW + 904-nm LPL, BW + 632-nm LED, and BW + 850-nm LED. The burn wound model was performed using a 100 °C copper plate, with 10 s of contact in the skin. The irradiations started 24 h after the lesion and were performed daily for 7 days. The burn wound groups showed an increase in the superoxide production, dichlorofluorescein, nitrites, and high protein oxidative damage. The activities of glutathione peroxidase and catalase were also increased, and a significant reduction in glutathione levels was observed compared to the control group. However, treatments with 660-nm LPL and 850-nm LED promoted protection against to oxidative stress, and similar results were also observed in the IL-6 and pERK1/2 expression. Taken together, these results suggest that LPL 660 nm and LED 850 nm appear reduced in the inflammatory response and oxidative stress parameters, thus decreasing dermal necrosis and increasing granulation tissue formation, in fact accelerating the repair of burn wounds.

Low-level laser therapy ameliorates disease progression in a mouse model of multiple sclerosis.

Multiple sclerosis (MS) is an autoimmune demyelinating inflammatory disease characterized by recurrent episodes of T cell-mediated immune attack on central nervous system (CNS) myelin, leading to axon damage and progressive disability. The existing therapies for MS are only partially effective and are associated with undesirable side effects. Low-level laser therapy (LLLT) has been clinically used to treat inflammation, and to induce tissue healing and repair processes. However, there are no reports about the effects and mechanisms of LLLT in experimental autoimmune encephalomyelitis (EAE), an established model of MS. Here, we report the effects and underlying mechanisms of action of LLLT (AlGaInP, 660 nm and GaAs, 904 nm) irradiated on the spinal cord during EAE development. EAE was induced in female C57BL/6 mice by immunization with MOG35-55 peptide emulsified in complete Freund's adjuvant. Our results showed that LLLT consistently reduced the clinical score of EAE and delayed the disease onset, and also prevented weight loss induced by immunization. Furthermore, these beneficial effects of LLLT seem to be associated with the down-regulation of NO levels in the CNS, although the treatment with LLLT failed to inhibit lipid peroxidation and restore antioxidant defense during EAE. Finally, histological analysis showed that LLLT blocked neuroinflammation through a reduction of inflammatory cells in the CNS, especially lymphocytes, as well as preventing demyelination in the spinal cord after EAE induction. Together, our results suggest the use of LLLT as a therapeutic application during autoimmune neuroinflammatory responses, such as MS.

The role of continuous versus fractionated physical training on muscle oxidative stress parameters and calcium-handling proteins in aged rats.

Age-associated decline in skeletal muscle mass and strength is associated with oxidative stress and Ca(2+) homeostasis disturbance. Exercise should be considered a viable modality to combat aging of skeletal muscle. This study aimed to investigate whether continuous and fractionated training could be useful tools to attenuate oxidative damage and retain calcium-handling proteins. We conducted the study using 24-month-old male Wistar rats, divided into control, continuous, and fractionated groups. Animals ran at 13 m min(-1) for five consecutive days (except weekends) for 6 weeks, for a total period of 42 days. Each session comprised 45 min of exercise, either continuous or divided into three daily sessions of 15 min each. Metabolic and oxidative stress markers, protein levels of mitochondrial transcription factors, and calcium-handling proteins were analyzed. Continuous exercise resulted in reduced ROS production as well as showed a decrease in TBARS levels and carbonyl content. On the other hand, fractionated training increased the antioxidant enzyme activities. The ryanodine receptor and phospholamban protein were regulated by continuous training while sodium calcium exchange protein was increased by the fractionated training. These data suggest that intracellular Ca(2+) can be modulated by various training stimuli. In addition, the modulation of oxidative stress by continuous and fractionated training may play an important regulatory role in the muscular contraction mechanism of aged rats, due to changes in calcium metabolism.

Physical Training Regulates Mitochondrial Parameters and Neuroinflammatory Mechanisms in an Experimental Model of Parkinson's Disease.

This study aimed to evaluate the effects of two different protocols for physical exercise (strength and aerobic training) on mitochondrial and inflammatory parameters in the 6-OHDA experimental model of Parkinson's disease. Six experimental groups were used (n = 12 per group): untrained + vehicle (Sham), strength training + vehicle (STR), treadmill training + vehicle (TTR), untrained + 6-OHDA (U + 6-OHDA), strength training + 6-OHDA (STR + 6-OHDA), and treadmill training + 6-OHDA (TTR + 6-OHDA). The mice were subjected to strength or treadmill training for 8 weeks. PD was induced via striatal injection of 6-OHDA 24 h after the last exercise session. Mice were euthanized by cervical dislocation and the striatum and hippocampus were homogenized to determine levels of tyrosine hydroxylase (TH), nuclear factor kappa B (NF-κB) p65, and sirtuin 1 (Sirt1) by western blot; tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), IL-17, interferon-γ (IFN-γ), and transforming growth factor ß1 (TGF-ß1) levels by ELISA; NO content; and complex I (CI) activity. STR + 6-OHDA mice had higher TH levels and CI activity and lower NF-κB p65 and IFN-γ levels in the striatum compared to U + 6-OHDA mice, while TTR + 6-OHDA mice had higher Sirt1 levels and CI activity in both the striatum and the hippocampus, compared to U + 6-OHDA mice. Strength training increased CI activity and TH and Sirt1 levels and reduced NO, NF-κB p65, TNF-α, IFN-γ, IL-1ß, and TGF-ß1 levels in 6-OHDA mice, while treadmill exercise increased CI activity and NO, TH, and Sirt1 levels and reduced NF-κB p65, TNF-α, IFN-γ, and IL-1ß levels. Our results demonstrated that both treadmill training and strength training promote neuroprotection, possibly by stimulating Sirt1 activity, which may in turn regulate both mitochondrial function and neuroinflammation via deacetylation of NF-κB p65. Changes in nitric oxide levels may also be a mechanism by which 6-OHDA-induced inflammation is controlled.

Gold nanoparticles and/or N-acetylcysteine mediate carrageenan-induced inflammation and oxidative stress in a concentration-dependent manner.

We report the effect of gold nanoparticles (AuNP) in an acute inflammation model induced by carrageenan (CG) and compared this effect with those induced by the antioxidant N-acetylcysteine (NAC) alone and by the synergistic effect of NAC and AuNP together. Male Wistar rats received saline or saline containing CG administered into the pleural cavity, and some rats also received NAC (20 mg/kg) subcutaneously and/or AuNP administered into the pleural cavity immediately after surgery. Four hours later, the rats were sacrificed and pleural exudates obtained for evaluation of cytokine levels and myeloperoxidase activities. Oxidative stress parameters were also evaluated in the lungs. The results demonstrated that the inflammatory process caused by the administration of CG into the pleural cavity resulted in a substantial increase in the levels of tumor necrosis factor-α, interleukin-1ß, and myeloperoxidase and a reduction in interleukin-10 levels. These levels seem to be reversed after different treatments in animals. Antioxidant enzymes exhibited positive responses after treatment of NAC + AuNP, and all treatments were effective at reducing lipid peroxidation and oxidation of thiol groups induced by CG. These findings suggest that small compounds, such as NAC plus AuNP, may be useful in the treatment of conditions associated with local inflammation.

Effects of phonophoresis and gold nanoparticles in experimental model of muscle overuse: role of oxidative stress.

The aim of the study described here was to investigate the effects of pulsed ultrasound and gold nanoparticles (AuNPs) on behavioral, inflammatory and oxidative stress parameters in an experimental model of overuse. Wistar rats performed 21 d of exercise on a treadmill at different intensities and were exposed to ultrasound in the presence or absence of AuNPs. The overuse model promoted behavioral changes and increased creatine kinase, superoxide dismutase and glutathione peroxidase activity, as well as the levels of superoxide, nitrotyrosine, nitric oxide, thiobarbituric acid reactive substance, carbonyl, tumor necrosis factor α and interleukin-6. These values were significantly decreased by AuNPs and by AuNPs plus ultrasound. Catalase activity remained unchanged and the glutathione level increased significantly after exposure to AuNPs plus ultrasound. These results suggest a susceptibility to anxiety as well as elevated levels of oxidative stress. However, therapeutic interventions with AuNPs plus ultrasound reduced the production of oxidants and oxidative damage and improved the anti-oxidant defense system.

Iontophoresis with gold nanoparticles improves mitochondrial activity and oxidative stress markers of burn wounds.

The aim of this study was to analyse the effects of microcurrent and gold nanoparticles on oxidative stress parameters and the mitochondrial respiratory chain in the healing of skin wounds. Thirty 60-day old male Wistar rats (250-300 g) were divided into five groups (N=6): Control; Burn wounds; Microcurrent (MIC); Gold nanoparticle gel (GNP gel) and Microcurrent+Gold nanoparticle gel (MIC+GNP gel). The microcurrent treatment was applied for five consecutive days at a dose of 300 µA. The results demonstrate a significant decrease in the activity of complexes I, II-III and IV in the Burn Wounds group compared to the control, and the MIC+GNP gel group was able to reverse this inhibition in complexes I, III and IV. Furthermore, a significant reduction in oxidative damage parameters and a significant increase in the levels of antioxidant defence enzymes were induced in the MIC+GNP gel group compared to the Burn Wounds group. The data strongly indicate that the group receiving treatment with MIC+GNP gel had improved mitochondrial functioning and oxidative stress parameters, which contributed to tissue repair.

The dose-dependent antioxidant effects of physical exercise in the hippocampus of mice.

Exercise increases both the consumption of oxygen and the production of reactive species in biological tissues, and this is counterbalanced by antioxidant adaptations to regular physical training. When the intensity of exercise fluctuates between mild and moderate, it improves the status of reduction-oxidation balance in the brain and induces neuroplasticity. However, intense exercise can oxidize the brain and impair neurological function. The effect of the frequency of exercise, which is an important factor in physical training, is still unknown. The effect of periodic exercise on biomarkers of oxidative stress in the hippocampus of mice was evaluated in this study. Mice were made to run on a treadmill for 8 weeks, two, three, or five times per week, and their hippocampi and quadriceps femoris muscles were then dissected. Biomarkers of oxidative damage were negatively correlated with the frequency of exercise and mitochondrial muscular activity, while the sulfhydryl contents were positively correlated with exercise frequency. A logistic analysis revealed a dose-dependent effect of exercise on these biomarkers. In summary, these results suggested that manipulating the frequency of physical exercise could induce antioxidant-related adaptations in the hippocampi of adult mice.

Impact of different resistance training protocols on muscular oxidative stress parameters.

This study analyzes oxidative stress in skeletal muscle using different resisted training protocols. We hypothesize that different types of training produce different specifics. To test our hypothesis, we defined 3 resistance training protocols and investigated the respective biochemical responses in muscle. Twenty-four male Wistar rats were distributed in 4 groups: untrained (UT), muscular resistance training (RT), hypertrophy training (HT), and strength training (ST). After 12 weeks of training on alternate days, the red portion of the brachioradialis was removed and the following parameters were assessed: lactate and glycogen content, superoxide production, antioxidant enzyme content, and activities (superoxide dismutase, SOD; catalase, CAT; GPx, glutathione peroxidase). Thiobarbituric acid-reactive substances (TBARS), carbonyl, and thiol groups were also measured. Results showed increased superoxide production (UT = 5.348 ± 0.889; RT = 5.117 ± 0,651; HT = 8.412 ± 0.431; ST = 6.354 ± 0.552), SOD (UT = 0.078 ± 0.0163; RT = 0.101 ± 0.013; HT = 0.533 ± 0.109; ST = 0.388 ± 0.058), GPx (UT = 0.290 ± 0.023; RT = 0.348 ± 0.014; HT = 0.529 ± 0.049; ST = 0.384 ± 0.038) activities, and content of GPx (HT = 3.8 times; ST = 3.0 times) compared with the UT group. CAT activity was lower (UT = 3.966 ± 0.670; RT = 3.474 ± 0.583; HT = 2.276 ± 0.302; ST = 2.028 ± 0.471) in HT and ST groups. Oxidative damage was observed in the HT group (TBARS = 0.082 ± 0.009; carbonyl = 0.73 ± 0.053; thiol = 12.78 ± 0.917) compared with the UT group. These findings indicate that HT causes an imbalance in oxidative parameters in favor of pro-oxidants, causing oxidative stress in skeletal muscle.