Plant hormones accumulation and its relationship with symplastic peroxidases expression during carnation-Fusarium oxysporum interaction

The vascular wilting caused by Fusarium oxysporum f. sp. dianthi (Fod) is the most relevant disease for carnation cultivation. Understanding the biochemical mechanisms involved in resistance to Fod will allow the development of new disease control strategies. In this research, the levels of some phytohormones such as salicylic acid (SA), methyl salicylate (MeSA), and methyl jasmonate (MeJA) were evaluated in symplast of carnation roots infected with this pathogen. The accumulation of these hormones was then correlated with the expression levels of symplastic peroxidases, enzymes involved in the plant resistance against pathogen during interaction. Our results suggested that pathogen infection causes a differential accumulation of SA, MeSA, and MeJA in a resistant cultivar (i.e. ‘Golem’), being earlier and higher than that observed in a susceptible one (i.e. ‘Solex’). Simultaneously, an increase of guaiacol peroxidase enzymatic activity (GPX) and transcriptional levels of a gene coding for a symplastic peroxidase were presented as part of the resistance response. The positive statistical correlation between the accumulation of SA and MeJA and the expression of peroxidases (GPX activity and mRNA levels) indicates the possible cellular relationship of these phenomena during the activation of the resistance to Fod. Our findings suggested some hormonal signaling mechanisms acting at the roots during the regulation of the biochemical response associated with resistance against Fod.

Relationship between indicators of insulin resistance and oxidative balancein adolescents with androgen deficiency

The purpose of the work was to study the relationship between the indicators of insulin resistance (IR), free radical oxidation products (FRO) levels, and the antioxidant system activity in adolescents with androgen deficiency (AD).Materials and methods. 58 adolescents 13­—18 years old with AD were examined. Serum levels of total testosterone, glucose, insulin, tiobarbituric acid active compounds (TBA), carbonylated proteins (CB), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activity were determined. The HOMA index and the coefficient of oxidative stress were calculated.Results and discussion. In the group of adolescents with AD without IR, an inverse correlation was found between the HOMA index and CAT activity. CAT activity negatively correlated with CB content and glucose concentration. In addition, an inverse relationship was found between the activity of GPO and SOD. IR indices indirectly, through feedback with the activity of CAT, influence to the formation of conditions for inhibition/activation of FRO of proteins.IR was revealed in 37.9 % of the examined adolescents with AD. Direct relationship was recorded between IR indicators and markers of oxidative stress, as well as between testosterone levels and GPx activity in the group of these patients. Direct correlation between the coefficient of oxidative stress and the content of TBA-­active compounds indicates the formation of oxidative stress due to the activation of lipid peroxidation. Reduced testosterone levels in adolescents with AD inhibits an increase in GPx activity and prevents compensation for excessive intensity of free radical processes. Conclusion. The results indicate that adolescents with AD have a close relationship between the processes of carbohydrate metabolism, FRO, and antioxidant protection.In adolescents with AD without IR, a balancebetween the studied parameterswas found.The formation of IR in adolescents with AD shifts the equilibrium of the oxidative balance towards the activation of FRO processes. Decreased testosterone levels in adolescents with AD do not maintain the body’s antioxidant status within normal limits.

Cadmium-Induced Kidney Injury in Mice Is Counteracted by a Flavonoid-Rich Extract of Bergamot Juice, Alone or in Association with Curcumin and Resveratrol, via the Enhancement of Different Defense Mechanisms

Cadmium (Cd) represents a public health risk due to its non-biodegradability and long biological half-life. The main target of Cd is considered the kidney, where it accumulates. No effective treatment for Cd poisoning is available so that several therapeutic approaches were proposed to prevent damages after Cd exposure. We evaluated the effects of a flavonoid-rich extract of bergamot juice (BJe), alone or in association with curcumin (Cur) and resveratrol (Re), in the kidney of mice exposed to cadmium chloride (CdCl2). Male mice were administered with CdCl2 and treated with Cur, Re, or BJe alone or in combination for 14 days. The kidneys were processed for biochemical, structural and morphometric evaluation. Cd treatment significantly increased urea nitrogen and creatinine levels, along with tp53, Bax, Nos2 and Il1b mRNA, while reduced that of Bcl2, as well as glutathione (GSH) content and glutathione peroxidase (GPx) activity. Moreover, Cd caused damages to glomeruli and tubules, and increased Nrf2, Nqo1 and Hmox1 gene expression. Cur, Re and BJe at 40 mg/kg significantly improved all parameters, while BJe at 20 mg/kg showed a lower protective effect. After treatment with the associations of the three nutraceuticals, all parameters were close to normal, thus suggesting a new potential strategy in the protection of renal functions in subjects exposed to environmental toxicants.

Glutathione peroxidase in acute coronary syndromes

<p>Glutathione peroxidase (GPx) and superoxide dismutase (SOD) are among the primary antioxidant enzymes that scavenge reactive oxygen species in the blood (ROS), thereby protecting against high levels of oxidative stress. The consequences of oxidative stress include cellular injury and tissue damage. High levels of oxidative stress have been implicated in the pathogenesis of acute coronary syndromes (ACS), however large clinical trials involving dietary antioxidant supplements have not shown a reduction in the rate of major adverse cardiovascular events (MACE). In a cohort of 262 ACS patients we examined the relationship between GPx activity, SOD activity and MACE. Patients with MACE were found to have significantly lower levels of GPx activity than those without MACE, whereas SOD activity did not differ between the groups. Furthermore, dividing the patients into quartiles corresponding to levels of GPx activity demonstrated significantly higher rates of MACE in the lower quartile of GPx activity compared to the highest quartile. Previous studies have demonstrated that deficiencies in GPx activity are associated with vascular dysfunction and platelet-dependent thrombosis, leading to the hypothesis that low levels of GPx activity would be associated with increased levels of platelet reactivity. In 51 ACS patients we did not observe a significant relationship between these two parameters, however we did demonstrate that increasing levels of GPx activity was associated with lower levels of ROS. ROS measures were based on the response of the platelets to addition of exogenous nitric oxide. Such an inverse relationship between GPx activity and levels of ROS is consistent with the view that GPx activity may play an important role in an ACS by reducing ROS-mediated damage, thereby protecting against MACE. We examined levels of GPx activity, protein concentration and mRNA expression across populations of ACS patients, stable coronary disease patients and healthy subjects. Cardiovascular risk factors thought to influence levels of GPx activity were controlled for in all three cohorts. These studies demonstrated that GPx activity, protein and mRNA levels were significantly elevated in the ACS patients compared to the stable coronary disease patients and healthy subjects. Oxidised low-density lipoprotein (oxLDL), a widely used marker of oxidative stress, was also significantly elevated in the ACS patients compared to the other two cohorts. In a study examining the temporal changes in GPx activity in the acute phase of an ACS, GPx activity was found to be highly dynamic, with no consistent single time point that identified when peak activity occurred. In the majority of patients, levels of oxLDL were found to peak prior to, or at the same time, as peak GPx activity, suggesting that GPx activity was modulated by changes in oxidative stress. In conclusion, the elevated levels of GPx activity observed in ACS patients were found to be highly dynamic throughout an ACS event. However those with lower levels of GPx activity have an increased risk of adverse clinical outcomes that may be due to an inadequate defence against levels of ROS. Whether these patients can be accurately identified and targeted with an appropriate therapeutic intervention warrants further investigation.</p>

Glutathione peroxidase in acute coronary syndromes

<p>Glutathione peroxidase (GPx) and superoxide dismutase (SOD) are among the primary antioxidant enzymes that scavenge reactive oxygen species in the blood (ROS), thereby protecting against high levels of oxidative stress. The consequences of oxidative stress include cellular injury and tissue damage. High levels of oxidative stress have been implicated in the pathogenesis of acute coronary syndromes (ACS), however large clinical trials involving dietary antioxidant supplements have not shown a reduction in the rate of major adverse cardiovascular events (MACE). In a cohort of 262 ACS patients we examined the relationship between GPx activity, SOD activity and MACE. Patients with MACE were found to have significantly lower levels of GPx activity than those without MACE, whereas SOD activity did not differ between the groups. Furthermore, dividing the patients into quartiles corresponding to levels of GPx activity demonstrated significantly higher rates of MACE in the lower quartile of GPx activity compared to the highest quartile. Previous studies have demonstrated that deficiencies in GPx activity are associated with vascular dysfunction and platelet-dependent thrombosis, leading to the hypothesis that low levels of GPx activity would be associated with increased levels of platelet reactivity. In 51 ACS patients we did not observe a significant relationship between these two parameters, however we did demonstrate that increasing levels of GPx activity was associated with lower levels of ROS. ROS measures were based on the response of the platelets to addition of exogenous nitric oxide. Such an inverse relationship between GPx activity and levels of ROS is consistent with the view that GPx activity may play an important role in an ACS by reducing ROS-mediated damage, thereby protecting against MACE. We examined levels of GPx activity, protein concentration and mRNA expression across populations of ACS patients, stable coronary disease patients and healthy subjects. Cardiovascular risk factors thought to influence levels of GPx activity were controlled for in all three cohorts. These studies demonstrated that GPx activity, protein and mRNA levels were significantly elevated in the ACS patients compared to the stable coronary disease patients and healthy subjects. Oxidised low-density lipoprotein (oxLDL), a widely used marker of oxidative stress, was also significantly elevated in the ACS patients compared to the other two cohorts. In a study examining the temporal changes in GPx activity in the acute phase of an ACS, GPx activity was found to be highly dynamic, with no consistent single time point that identified when peak activity occurred. In the majority of patients, levels of oxLDL were found to peak prior to, or at the same time, as peak GPx activity, suggesting that GPx activity was modulated by changes in oxidative stress. In conclusion, the elevated levels of GPx activity observed in ACS patients were found to be highly dynamic throughout an ACS event. However those with lower levels of GPx activity have an increased risk of adverse clinical outcomes that may be due to an inadequate defence against levels of ROS. Whether these patients can be accurately identified and targeted with an appropriate therapeutic intervention warrants further investigation.</p>

Sex-specific association between antioxidant defense system and therapeutic response to risperidone in schizophrenia: a prospective longitudinal study

: There are various differences in the response to different antipsychotics and antioxidant defense system (ADS) by sex. Previous studies have shown that several ADS enzymes are closely related to the treatment response of patients with antipsychotics-naïve first-episode (ANFE) schizophrenia. Therefore, the main goal of this study was to assess the sex difference in the relationship between changes in ADS enzyme activities and risperidone response. The plasma activities of glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD) and total antioxidant status (TAS) were measured in 218 patients and 152 healthy controls. Patients were treated with risperidone for 3 months, and we measured PANSS for psychopathological symptoms and ADS biomarkers at baseline and at the end of 3 months of treatment. We compared sex-specific group differences between 50 non-responders and 168 responders at baseline and at the end of the three months of treatment. We found that female patients responded better to risperidone treatment than male patients. At baseline and 3-month follow-up, there were no significant sex differences in TAS levels and three ADS enzyme activities. Interestingly, only in female patients, after 12 weeks of risperidone treatment, the GPx activity of responders was higher than that of non-responders. These results indicate that after treatment with risperidone, changes in GPx activity were associated with treatment response, suggesting that changes in GPx may be a predictor of response to risperidone treatment in female patients with ANFE schizophrenia.

Hydroxy-selenomethionine as an organic source of selenium in the diet improves boar reproductive performance in artificial insemination programs

This study aimed to compare different selenium (Se) sources in the diet on boar's semen quality and fertility. For this, 28 boars aged 8 to 28 months were fed with the following dietary treatments for 95 days: 0.3 mg Se/kg as sodium selenite (SS, n = 14) and 0.3 mg Se/kg as hydroxy-selenomethionine (OH-SeMet, n = 14). During this period, two experiments were carried out. In experiment 1, the semen of all boars was evaluated every 2 weeks. Raw semen was initially evaluated for the processing of seminal doses, which were stored at 17 °C for 72 h, followed by sperm quality assessments. Furthermore, Se concentration and glutathione peroxidase (GPx) activity were measured in the seminal plasma. In experiment 2, 728 females were inseminated weekly with seminal doses from boars of the different experimental groups to further assess in vivo fertility and litter characteristics. Results demonstrated that boars fed OH-SeMet had more Se in their seminal plasma (p &lt; 0.05), showing the greater bioavailability of the organic source in the male reproductive system. Moreover, boars fed OH-SeMet tended (p &lt; 0.10) towards a higher total sperm count in the ejaculate (66.60 vs. 56.57 × 10 9 sperm), and the number of seminal doses (22.11 vs. 18.86; 3 × 10 9 sperm/dose) when compared to those fed SS. No effect of the dietary treatments was observed on GPx activity in seminal plasma (p &gt; 0.05), as well as on raw and stored semen quality (p &gt; 0.05). Under in vivo conditions, seminal doses from boars fed OH-SeMet tended (p &lt; 0.10) towards a higher pregnancy rate at weeks 3, 5, and 8, and also resulted in a higher (p &lt; 0.05) percentage of pregnant females in the overall period (99.30 vs. 97.00). In conclusion, the replacement of SS with OH-SeMet in boars' diet can improve sperm production and results in better reproductive performance for them, bringing greater productivity and profitability to artificial insemination centers and commercial pig farms.

Evaluation of oxidative stress biomarkers in acute mercury intoxication

Objective:&nbsp;Very few studies have evaluated the association between mercury exposure and oxidative stress in humans, particularly in children. This is the first report where we aimed to determine the oxidative stress status of children who were accidently exposed to elemental mercury. Methods: In the present study, the study group was composed of 86 randomly selected children poisoned by mercury; the control group was composed of 78 children who had no history of mercury exposure. At admission, blood samples were collected. Blood superoxide dismutase activity, catalase enzyme activity, and glutathione peroxidase activity were measured by Fridovich, Beutler, and Lawrence Burk methods respectively, and the results were given as U/g Hb . Malondialdehyde level was measured by Ohkawa methods , and the results were given as mmol/ml. Results:&nbsp;Catalase levels were significantly lower in the patient group compared to the control group (1.28&plusmn;0.62 vs 3.90 &plusmn; 0.86 U/g Hb, p<0.01). In exposed children, SOD levels were significantly higher than the controls (5936 &plusmn; 810 vs 2226 &plusmn; 464 U/g Hb, p<0,05), while the GPx activity was significantly lower (13.01 &plusmn; 3.21&nbsp; vs 34.97 &plusmn; 7.32 U/g Hb, p<0.01). The MDA levels of the mercury group were significantly higher than the MDA levels of the control group (2.85&plusmn;0.84&nbsp; vs 2.05&plusmn;0.79 mmol/ml, p<0.05) . Conclusion: The results of the present study showed that acute mercury poisoning causes alteration of oxidative stress status in children exposed to elemental mercury.

1,25(OH)2D3 Inhibited Ferroptosis in Zebrafish Liver Cells (ZFL) by Regulating Keap1-Nrf2-GPx4 and NF-κB-hepcidin Axis

Ferroptosis is a kind of iron-dependent programed cell death. Vitamin D has been shown to be an antioxidant and a regulator of iron metabolism, but the relationship between vitamin D and ferroptosis is poorly studied in fish. This study used zebrafish liver cells (ZFL) to establish a ferroptosis model to explore the effect of 1,25(OH)2D3 on cell ferroptosis and its mechanism of action. The results showed that different incubation patterns of 1,25(OH)2D3 improved the survival rate of ZFL, mitigated mitochondrial damage, enhanced total glutathione peroxidase (GPx) activity, and reduced intracellular reactive oxygen species (ROS), lipid peroxidation (LPO), and malondialdehyde (MDA), as well as iron ion levels, with the best effect at 200 pM 1,25(OH)2D3 preincubation for 72 h. Preincubation of ZFL at 200 pM 1,25(OH)2D3 for 72 h downgraded keap1 and ptgs2 gene expression, increased nrf2, ho-1, fth1, gpx4a,b expression, and lowered the expression of the nf-κb p65,il-6,il-1β gene, thus reducing the expression of hamp1. The above results indicate that different incubation patterns of 1,25(OH)2D3 have protective effects on ferroptosis of ZFL induced by ferroptosis activator RSL3 and 1,25(OH)2D3 can inhibit ferroptosis of ZFL by regulating Keap1–Nrf2–GPx4 and NF-κB–hepcidin axis.

Montelukast Protects Against Renal Damage Due to Cadmium Toxicity: In vivo and In vitro Experiments

Background: The protective effects of Montelukast (Mont), as an anti-inflammatory drug, against cadmium-induced kidney cell damage have already been studied and identified. Since the significant part of cadmium nephrotoxicity is caused by oxidative stress, this in vivo and in vitro study was conducted to investigate the possible role of Montelukast antioxidant properties in the protection. Methods: In the in vivo section, 42 rats were treated in seven groups of six rats as follows: Control; Cadmium Chloride (CdCl2) control; Montelukast control; CdCl2 plus Montelukast treatment; CdCl2 with Montelukast pre-treatment; Vitamin E control; CdCl2 plus Vitamin E treatment. In the in vitro section, human embryonic kidney cells (HEK293) were treated with CdCl2; Montelukast; Combined CdCl2 and Montelukast; Vitamin E; Combined CdCl2 and Vitamin E. Results: Montelukast, in both treatment and pretreatment forms, reduced serum urea, creatinine, and potassium levels compared to CdCl2 group, in vivo. Similar to vitamin E, the pre-treatment with Montelukast was associated with a significant decrease in Nitric Oxide (NO) and Total Antioxidant Capacity (TAC) in serum and renal tissue, and a significant increase in Glutathione Peroxidase (GPX) activity in serum compared those in the CdCl2 group. In the in vitro section of the study, Montelukast significantly reduced Malondialdehyde (MDA) and NO while the TAC level, Superoxide Dismutase (SOD), and the GPX activity increased significantly. Conclusion: Overall, the antioxidant effects of Montelukast appear to play a prominent role in preventing the renal toxicity due to cadmium exposure.