Generation Of Species Research Articles

Evaluation of Sinapic Acid to Ameliorate Ionizing Radiation Induced Peripheral Blood Mononuclear Cell Death

Introduction: The UV radiation is known as a potential environmental carcinogen which causes damages of macromolecules like DNA, RNA, lipid, and protein inside the cell and eventually causes cell death. Persons who chronically exposed to UV radiation due to occupational or environmental exposure have a potential risk to develop cancer of the skin and internal organs. Polyphenols have a promising role in scavenging reactive oxygen species developed in our body due to a variety of exposure including radiation. In the present study, we are therefore evaluating the role of sinapic acid (SA), a polyphenol, in scavenging UV radiation-induced generation of reactive oxygen species and eventual cell death. We have studied the biological activity of SA as a potential antioxidant on human peripheral blood mononuclear cells taken from human volunteers. Methods : Graded concentration of SA in different solvent mediums was applied to UV exposed peripheral blood mononuclear cells for evaluating the best effective delivery system and concentration against UV radiation. Result: After series of experiments, we have observed that even at 10 µM concentration, SA is effective against UV induced cellular death. Conclusion: Finally, from this work we are inviting lots of works in this field to establish this molecule as a medicine to reduce radiation-induced cellular death.

Anaerobic RSH-dependent tellurite reduction contributes to Escherichia coli tolerance against tellurite

BackgroundTellurium is a rare metalloid that exerts high toxicity on cells, especially on bacteria, partly due to reactive oxygen species (ROS) generation. Moreover, it has also been observed that tellurite can target free cell thiols groups (RSH) (i.e. reduced glutathione (GSH)), enhancing the cellular redox imbalance. Additionally, in vitro experiments have suggested that several enzymes can reduce tellurite (IV) to its elemental form (0); where RSH present on their active sites may be responsible for the process. Nevertheless, the mechanisms implemented by bacteria for tellurite reduction and its role in resistance have not been evaluated in vivo.ResultsThis work shows that tellurite reduction to elemental tellurium is increased under anaerobic conditions in E. coli cells. The in vivo tellurite reduction is related to the intracellular concentration of total RSH, in the presence and absence of oxygen. This metabolization of tellurite directly contributes to the resistance of the bacteria to the oxyanion.ConclusionsWe demonstrated that in vivo tellurite reduction is related to the intracellular thiol concentration, i.e. large availability of cellular RSH groups, results in a more significant reduction of tellurite. Furthermore, we observed that, when the bacterium exhibits less resistance to the oxyanion, a decreased tellurite reduction was seen, affecting the growth fitness. Together, these results let us propose that tellurite reduction and the intracellular RSH content are related to the oxyanion bacterial resistance, this tripartite mechanism in an oxygen-independent anaerobic process.

Mechanistic study of silica nanoparticles on the size-dependent retinal toxicity in vitro and in vivo

BackgroundSilica nanoparticles (SiO2 NPs) are extensively applied in the biomedical field. The increasing medical application of SiO2 NPs has raised concerns about their safety. However, studies on SiO2 NP-induced retinal toxicity are lacking.MethodsWe investigated the retinal toxicity of SiO2 NPs with different sizes (15 and 50 nm) in vitro and in vivo along with the underlying mechanisms. The cytotoxicity of SiO2 NPs with different sizes was assessed in R28 human retinal precursor cells by determining the ATP content and LDH release. The cell morphologies and nanoparticle distributions in the cells were analyzed by phase-contrast microscopy and transmission electron microscopy, respectively. The mitochondrial membrane potential was examined by confocal laser scanning microscopy. The retinal toxicity induced by SiO2 NPs in vivo was examined by immunohistochemical analysis. To further investigate the mechanism of retinal toxicity induced by SiO2 NPs, reactive oxygen species (ROS) generation, glial cell activation and inflammation were monitored.ResultsThe 15-nm SiO2 NPs were found to have higher cytotoxicity than the larger NPs. Notably, the 15-nm SiO2 NPs induced retinal toxicity in vivo, as demonstrated by increased cell death in the retina, TUNEL-stained retinal cells, retinal ganglion cell degeneration, glial cell activation, and inflammation. In addition, The SiO2 NPs caused oxidative stress, as demonstrated by the increase in the ROS indicator H2DCF-DA. Furthermore, the pretreatment of R28 cells with N-acetylcysteine, an ROS scavenger, attenuated the ROS production and cytotoxicity induced by SiO2 NPs.ConclusionsThese results provide evidence that SiO2 NPs induce size-dependent retinal toxicity and suggest that glial cell activation and ROS generation contribute to this toxicity.Graphical

Chromosomal aberrations, DNA damage, and biochemical disturbances induced by silver nanoparticles in mice: role of particle size and natural compounds treatment

Context Nanotechnology is widely used nowadays in several fields of industry, engineering, and medicine, the biological action mechanisms of AgNPs, which mainly involve the release of silver ions (Ag+), generation of reactive oxygen species (ROS). Objective The potential toxicity AgNPs of damages to hepatic cells, hesperidin, and naringin role for their protective effect against the increase of ROS due to AgNPs toxicity. They can be restored, most cellular biochemical parameters, genotoxicity, mutagenicity, and histopathological analysis. Materials and methods Toxicity was induced by an oral dose of Ag NPs of (20–100 nm) for one month, after that treated with hesperidin, naringin (100 mg/kg) for three weeks, malondialdehyde (MDA) levels, nitric oxide (NO), glutathione (GSH) and catalase were estimated. Also, aminotransferases (AST and ALT), alkaline phosphatase (ALP), γ-glutamyltransferase (GGT), albumin, and total bilirubin were determined, following Chromosomal aberrations, DNA breaks, and histological analyses Results hesperidin, and naringin treatment, recorded amelioration in most biochemical, genetic, and spermatogenesis disturbances Also, histological Investigations were improved. Conclusion Their biological safety problems, such as potential toxicity on cells, tissue, and organs should be paid enough attention, hesperidin and naringin amelioration fundamental alterations, as hepatic architectural and DNA damage, related to its role as an antioxidant and anti-inflammatory agent.

Lipopolysaccharide and ARDS caused by new coronavirus infection: hypotheses and facts

This review presents data from the literature that provide insight into the role of the lipopolysaccharide (LPS) of the Gram-negative bacteria in pathogenesis of acute respiratory distress syndrome (ARDS) caused by the novel SARS-CoV-2 coronavirus infection. ARDS is a syndrome of severe respiratory failure, an acutely occurring diffuse inflammatory lesion of lung tissue that develops as a nonspecific reaction to various direct (aspiration, inhalation of toxic gases), and systemic (sepsis, polytrauma) damaging factors and leading to development of acute respiratory failure (ARF), due to impaired structure of the lung parenchyma, disturbances in vascular permeability, decreased area of ventilated lung tissue. ARDS from coronavirus infection appears to have worse outcomes than ARDS from other causes. Mortality from typical ARDS at the intensive care units and hospitals is 35.3% and 40.0%, respectively, while the lethality rates for COVID-19-associated ARDS, ranged from 26% to 61.5%. Among patients who underwent artificial ventilation of the lungs, the mortality rates can range from 65.7% to 94%. Risk factors for poor outcomes include, e.g., older age, presence of concomitant diseases such as hypertension, cardiovascular disease and diabetes mellitus; decreased number of lymphocytes, kidney injury, and increased D-dimer levels. Death with ARDS in COVID-19 occurs as a result of respiratory failure (53%), respiratory failure combined with heart failure (33%), myocardial damage and circulatory failure (7%), or death from an unknown cause. A large number of studies show that bacterial LPS is directly or indirectly involved in all pathogenetic links of ARDS caused by the SARS-CoV-2 virus, i.e., worsening the course of inflammatory lung diseases due to decreased level of angiotensin-converting enzyme 2 (ACE2); increasing generation of reactive oxygen species (ROS) via NADPH oxidase and subsequent inactivation of endothelial nitric oxide synthase (eNOS) and decreasing bioavailability of endothelial NO, thus leading to endothelial dysfunction; interacting with proteins of surfactants. SP-A and SP-D, promoting early destruction of the cellular monolayers and lowering surface tension, interact with soluble CD14 receptor, which also has a pro-inflammatory effect on epithelial and endothelial cells, leading to p38MAPK activation via TLR4 receptors, causing degradation of IêBá protein and subsequent translocation of p65 NF-êB into the nucleus, thus inducing transcription of IL-6 and adhesion molecules (ICAM-1, VCAM-1 and E-selectin), and, as shown by Petruk et al. (2020), causing direct binding to the viral S protein in combination with LPS, thus enhancing activation of nuclear factor-kappa B (NF-êB) in monocytic THP-1 cells and cytokine responses in mononuclear blood cells. These pathophysiological mechanisms require further in-depth study in order to understand the nature of changes that occur in the patients with new SARS-CoV-2 infection.

Testosterone Contributes to Vascular Dysfunction in Young Mice Fed a High Fat Diet by Promoting Nuclear Factor E2-Related Factor 2 Downregulation and Oxidative Stress.

Obesity, an important risk factor for cardiovascular disease, promotes vascular oxidative stress. Considering that free testosterone levels remain within the reference range, especially in obese young men and that testosterone stimulates reactive oxygen species (ROS) generation, we sought to investigate whether testosterone interferes with obesity-associated oxidative stress and vascular dysfunction in male mice. We hypothesized that testosterone favors ROS accumulation and vascular dysfunction in high fat diet (HFD)-fed obese mice. We also questioned whether testosterone downregulates the nuclear factor E2–related factor 2 (Nrf2), one of the major cellular defense mechanisms against oxidative stimuli. Male C57Bl/6J mice were submitted to orchiectomy or sham-operation. Mice received either a control diet (CD) or HFD for 18 weeks. Vascular function was assessed in thoracic aortic rings and molecular mechanisms by which testosterone contributes to vascular dysfunction were determined. HFD reduced acetylcholine-induced vasodilation and increased vascular ROS generation in sham mice. Castration prevented these effects. Treatment of castrated mice fed either the CD or HFD with testosterone propionate decreased acetylcholine vasodilation. HFD decreased Nrf2 nuclear accumulation, events linked to decreased mRNA expression and activity of Nrf2-regulated enzymes (catalase, heme oxygenase-1, peroxiredoxin, and thioredoxin). These events were prevented in HFD-fed castrated mice. Bardoxolone, a Nrf2 activator, increased nuclear accumulation of Nrf2, decreased ROS generation and improved acetylcholine vasodilation in HFD-fed sham mice. In vitro, testosterone increased ROS generation and decreased Nrf2 nuclear accumulation. These effects were prevented in the presence of an androgen receptor antagonist, an inhibitor of gene transcription and an inhibitor of the pro-oxidant enzyme NOX-1. These results indicate that testosterone downregulates Nrf2, leading to oxidative stress and vascular dysfunction in HFD-fed obese young mice.

Biosynthesis of zinc oxide nanoparticles from Phyllanthus Niruri plant extract for photocatalytic and antioxidant activities

ABSTRACT The lack of access to hygienic conditions and clean water is a serious issue in developing countries. Eco-friendly, bio-synthesised nanomaterials-based catalyst will be potential candidate material for waste water treatment. In this study, Phyllanthus niruri plant extract was used to make non-toxic, cost-effective ZnO NPs. The X-ray diffraction pattern was shown that the bio-synthesised ZnO NPs were in hexagonal wurtzite structure. The SEM image was used to analyse the surface morphology of the NPs, and the chemical purity of the NPs was analysed by EDAX spectrum. The various functional groups that exist in the NPs and purity of the prepared samples were analysed by Fourier-transform infrared (FTIR) spectroscopy. The bio-synthesised ZnO NPs decolourised the methylene blue dye and Reactive Red 120. The larger surface area of ZnO nanoparticles (NPs) and wide absorption band of the NPs led to superior photocatalytic activity under the sunlight irradiation. The bio-synthesised ZnO NPs prevented or slowed down the oxidative damage of cells by controlling the generation of reactive oxygen species (ROS).

Modelling biophoton emission kinetics based on the initial intensity value in Helianthus annuus plants exposed to different types of stress

Biophoton radiation also referred to as ultra-weak photon emission (UPE) is used to denote a spontaneous and permanent photon emission associated with oxidative processes in cells and seems to universally occur in all living systems as a result of the generation of reactive oxygen species (ROS) that are produced under stress conditions. The measurement of this biophoton emission allows for a non-invasive approach in monitoring phenological stages throughout plant development which has direct relevance in agriculture research. In this study, the emission of photons emanating from sunflower (Helianthus annuus, L.) plants exposed to biotic and abiotic stress has been investigated. In healthy plants raised under controlled growth conditions UPE was low whereas in stressed individuals it considerably increased; particularly upon water stress. The kinetics of the signal is shown to reveal an exponential decay with characteristic dynamics, which appears to reflect different physiological states concomitantly setting in upon stress. The dynamics of the signal decay is shown to vary according to the type of stress applied (biotic vs. abiotic) hence suggesting a putative relationship between the kinetic traits of change in the signal intensity-decay and stress. Intriguingly, the determination of the change in the intensity of biophoton emission that ensued in a short time course was possible by using the initial biophoton emission intensity. The predictability level of the equations demonstrated the applicability of the model in a corroborative manner when employing it in independent UPE-measurements, thus permitting to forecast the intensity change in a very accurate way over a short time course. Our findings allow the notion that albeit stress confers complex and complicated changes on oxidative metabolism in biological systems, the employment of biophoton imaging offers a feasible method making it possible to monitor oxidative processes triggered by stress in a non-invasive and label-free way which has versatile applications especially in precision agriculture.

Trypanosoma cruzi Mitochondrial Peroxiredoxin Promotes Infectivity in Macrophages and Attenuates Nifurtimox Toxicity.

Trypanosoma cruzi is the causative agent of Chagas disease which is currently treated by nifurtimox (NFX) and benznidazole (BZ). Nevertheless, the mechanism of action of NFX is not completely established. Herein, we show the protective effects of T. cruzi mitochondrial peroxiredoxin (MPX) in macrophage infections and in response to NFX toxicity. After a 3-day treatment of epimastigotes with NFX, MPX content increased (2.5-fold) with respect to control, and interestingly, an MPX-overexpressing strain was more resistant to the drug. The generation of mitochondrial reactive species and the redox status of the low molecular weight thiols of the parasite were not affected by NFX treatment indicating the absence of oxidative stress in this condition. Since MPX was shown to be protective and overexpressed in drug-challenged parasites, non-classical peroxiredoxin activity was studied. We found that recombinant MPX exhibits holdase activity independently of its redox state and that its overexpression was also observed in temperature-challenged parasites. Moreover, increased holdase activity (2-fold) together with an augmented protease activity (proteasome-related) and an enhancement in ubiquitinylated proteins was found in NFX-treated parasites. These results suggest a protective role of MPX holdase activity toward NFX toxicity. Trypanosoma cruzi has a complex life cycle, part of which involves the invasion of mammalian cells, where parasite replication inside the host occurs. In the early stages of the infection, macrophages recognize and engulf T. cruzi with the generation of reactive oxygen and nitrogen species toward the internalized parasite. Parasites overexpressing MPX produced higher macrophage infection yield compared with wild-type parasites. The relevance of peroxidase vs. holdase activity of MPX during macrophage infections was assessed using conoidin A (CA), a covalent, cell-permeable inhibitor of peroxiredoxin peroxidase activity. Covalent adducts of MPX were detected in CA-treated parasites, which proves its action in vivo. The pretreatment of parasites with CA led to a reduced infection index in macrophages revealing that the peroxidase activity of peroxiredoxin is crucial during this infection process. Our results confirm the importance of peroxidase activity during macrophage infection and provide insights for the relevance of MPX holdase activity in NFX resistance.

Wogonin inhibits tight junction disruption via suppression of inflammatory response and phosphorylation of AKT/NF-κB and ERK1/2 in rhinovirus-infected human nasal epithelial cells.

The maintenance of tight junction integrity contributes significantly to epithelial barrier function. If barrier function is destroyed, cell permeability increases and the movement of pathogens is promoted, further increasing the susceptibility to secondary infection. Here, we examined the protective effects of wogonin on rhinovirus (RV)-induced tight junction disruption. Additionally, we examined the signaling molecules responsible for anti-inflammatory activities in human nasal epithelial (HNE) cells. Primary HNE cells grown at an air-liquid interface and RPMI 2650 cells were infected apically with RV. Incubation with RV resulted in disruption of tight junction proteins (ZO-1, E-cadherin, claudin-1, and occludin) in the HNE cells. Cell viability of wogonin-treated HNE cells was measured using the MTT assay. Pretreatment with wogonin decreased RV-induced disruption of tight junctions in HNE cells. Furthermore, wogonin significantly decreased RV-induced phosphorylation of Akt/NF-κB and ERK1/2. Additionally, RV-induced generation of reactive oxygen species and RV-induced up-regulation of the production of inflammatory cytokines IL-8 and IL-6 were diminished by wogonin in HNE cells. Wogonin inhibits HRV-induced tight junction disruption via the suppression of inflammatory responses and phosphorylation of Akt/NF-κB and ERK1/2 in HNE cells. These finds will facilitate the development of novel therapeutic strategies.

Dual optogenetic generation and detection of reactive oxygen species throughout mitochondrial microdomains

Dual optogenetic generation and detection of reactive oxygen species throughout mitochondrial microdomains

VILI Induced Nitration of RhoA Disrupts Mitochondrial Function Through Increased Generation of Reactive Oxygen Species

VILI Induced Nitration of RhoA Disrupts Mitochondrial Function Through Increased Generation of Reactive Oxygen Species

Ferulic acid protects renal tubular epithelial cells against anoxia/reoxygenation injury mediated by AMPKα1

Anoxia/reoxygenation (A/R) injury causes dysfunction of rat renal tubular epithelial cells (NRK-52E), which is associated with excess reactive oxygen species (ROS) generation and eventually leads to apoptosis. Ferulic acid (FA), a phenolic acid, which is abundant in fruits and vegetables. FA possesses the properties of scavenging free radicals and cytoprotection against oxygen stress. In the study, the protective effects of FA against NRK-52E cells damage induced by A/R were explored and confirmed the role of AMP-activated protein kinaseα1 (AMPKα1). We found that after NRK-52E cells suffered A/R damage, FA pretreatment increased the cell viability and decreased LDH activity in culture medium in a concentration-dependent manner, the activities of endogenous antioxidant enzymes such as glutathione peroxidase, superoxide dismutase and catalase improved, intracellular ROS generation and malondialdehyde contents mitigated. In addition, pretreatment of 75 μM FA ameliorated mitochondrial dysfunction by A/R-injury and ultimately decreased apoptosis (25.3 ± 0.61 vs 12.1 ± 0.60), which was evidenced by preventing the release of cytochrome c from mitochondria to the cytoplasm. 75 μM FA pretreatment also significantly upregulated AMPKα1 expression (3.16 ± 0.18 folds) and phosphorylation (2.56 ± 0.13 folds). However, compound C, a specific AMPK inhibitor, significantly attenuated FA pretreatment’s effects, as mentionedabove. These results firstly clarified that FA pretreatment attenuated NRK-52E cell damage induced by A/R via upregulating AMPKα1 expression and phosphorylation.

SIGNALING ROLE OF REACTIVE OXYGEN SPECIES IN PLATELETS

Abstract: Review. Reactive oxygen species are formed as a result of redox reactions and are involved in signaling associated with cell growth, differentiation, and death. Platelets are both a source and a target of reactive oxygen species. The review regards the molecular mechanisms of the reactive oxygen species formation under platelet activation conditions and effects of altered redox balance on platelet function. The main platelet sources of reactive oxygen species are isoforms of NADPH oxidases, cyclooxygenase, xanthine oxidase, and mitochondrial electron transport chain. Reactive oxygen species produced during platelet activation by agonists act as secondary messengers and can interfere with signaling pathways that enhance agonist-induced platelet activation. The signaling pathway mediated by glycoprotein VI, the main platelet receptor for collagen, leading mainly to the generation of intracellular reactive oxygen species, as well as the signaling pathway activated by thrombin, leading to the production of extracellular reactive oxygen species are considered. Extracellular reactive oxygen species enhance initial signaling and support platelet recruitment and activation. Activated platelets are involved in the coupling of thrombosis, inflammation, and innate immune responses. The platelet antioxidant systems play an important role in preventing the cytotoxic effects of reactive oxygen species, as well as in the regulation of platelet signaling pathways. The authors of the review and other researchers have shown that the redox status of platelets can serve as a biomarker in the studies on prevention and treatment of diseases involving oxidative stress and can be used for objective assessments of the patients' condition severity (including depression and schizophrenia, in which the authors found a decrease in the activity of platelet glutathione -dependent antioxidant enzymes).

The expression and survival significance of sodium glucose transporters in pancreatic cancer

BackgroundSodium glucose transporters (SGLTs) play vital roles in glucose uptake in many solid cancers, including pancreatic cancer (PC). However, their expression profile in pancreatic cancer and correlation with prognosis are not clear. Thus, we aimed to analyse the expression profile and prognostic significance of SGLT-1 and SGLT-2 in PC.MethodsEighty-eight patients with pancreatic ductal adenocarcinoma (PDAC) undergoing surgery in Huashan Hospital, Fudan University, from July 2017 to June 2020 were enrolled in the study. Specimens for immunohistochemistry were obtained through surgical resection. Bioinformatics analysis was performed based on the Gene Expression Omnibus (GEO), Oncomine and The Cancer Genome Atlas (TCGA) databases. The statistics were calculated using IBM SPSS Statistics, version 20 and R 4.1.1. P values lower than 0.05 were considered to indicate statistical significance.ResultsSGLT-1 but not SGLT-2 was significantly overexpressed in PDAC. Survival analysis showed that the median overall survival (OS) and progression-free survival (PFS) of patients with high SGLT-1 expression were significantly longer than that of patients with low SGLT-1 expression. Cox regression indicated that high SGLT-1 expression was an independent predictor for a better prognosis, while residual tumour status (R1 and R2) was an independent risk factor for a poor prognosis. Finally, PDZK1-interacting protein 1 (PDZK1IP1), a protein participating in the generation of reactive oxygen species, was overexpressed in PDAC and its expression was significantly correlated with SGLT-1.ConclusionsSGLT-1 but not SGLT-2 was overexpressed in PDAC, and the overexpression of SGLT-1 could be a predictor of a better prognosis. Residual tumour status (R1 and R2) was a risk factor for poor prognosis and disease progression.

Ferric Ammonium Citrate Upregulates PD-L1 Expression through Generation of Reactive Oxygen Species.

Iron plays an important role in macrophage polarization by altering metabolic and redox status. However, the impact of iron on the immune status of macrophages is still controversial. In this study, we report that ferric ammonium citrate (FAC) upregulates PD-L1 expression in macrophages. FAC not only altered the phenotype of macrophages but also led to enriching immune-modulatory T cell subsets. Since iron is known to be a constituent of coenzymes facilitating metabolic processes in mitochondria, we examined the metabolic status of FAC-overloaded macrophages by measuring the oxygen consumption rate (OCR) and the represented coenzyme, aconitase. In addition to enhancement of metabolic processes, FAC accelerated the Fenton reaction in macrophages, which also contributed to the facilitation of oxygen consumption. We reasoned that the enhancement of the OCR leads to the production of reactive oxygen species (ROS), which are directly linked to PD-L1 induction. Using ferrostatin, rotenone, and N-acetyl-L-cysteine, we confirmed that metabolic and redox regulation is responsible for FAC-mediated PD-L1 expression. Furthermore, we suggested that FAC-induced ROS production may explain FAC-mediated pro- and anti-inflammatory responses in macrophages. These findings may extend our understanding of regulating iron concentration during immune checkpoint therapy in cancer patients.

Attenuation Effect of Salvianolic Acid B on Testicular Ischemia-Reperfusion Injury in Rats.

During testicular ischemia-reperfusion, overproduction of reactive oxygen species is associated with testicular injury. We injected hydrogen peroxide (a representative of reactive oxygen species) into normal testis via the testicular artery. The experiment demonstrates that reactive oxygen species can cause spermatogenic injury. Salvianolic acid B, the most abundant bioactive component in Salvia miltiorrhiza Bunge, has been reported to possess a potent antioxidant activity. This study was conducted to evaluate the effect of salvianolic acid B on testicular ischemia-reperfusion injury in a rat testicular torsion-detorsion model. Rats were randomly separated into three groups, including 20 rats in each group: control group with sham operation, testicular ischemia-reperfusion group, and testicular ischemia-reperfusion + salvianolic acid B-treated group. In the testicular ischemia-reperfusion group, left testicular torsion of 720° for 2 hours was induced, and then testicular detorsion was carried out. Rats in the salvianolic acid B-treated group additionally had salvianolic acid B administered intravenously at detorsion. At 4 hours after detorsion, testes of 10 rats from each group were collected to analyze the protein expression of xanthine oxidase which catalyzes generation of reactive oxygen species and malondialdehyde concentration (an indirect indicator of reactive oxygen species). At 3 months after detorsion, testes of the remaining 10 rats from each group were collected to analyze spermatogenesis. Compared with the control group, xanthine oxidase protein expression and malondialdehyde concentration in ipsilateral testes of testicular ischemia-reperfusion group increased significantly, while spermatogenesis decreased significantly. In the salvianolic acid B-treated group, xanthine oxidase protein expression and malondialdehyde concentration in ipsilateral testes decreased significantly, while spermatogenesis increased significantly, compared with the testicular ischemia-reperfusion group. These results suggest that salvianolic acid B can attenuate testicular torsion/detorsion-induced ischemia/reperfusion injury by downregulating the xanthine oxidase protein expression to inhibit reactive oxygen species formation.

Metal biomonitoring using fractioned dust to investigate urinary and oxidative stress biomarkers among occupationally exposed chromite mine workers.

Exposure to heavy metals has been associated with the generation of reactive oxygen species (ROS) among exposed individuals in occupational and environmental settings. Dust is considered a significant contributor to airborne metal exposure, and previous data suggest that their levels in dust may vary based on its particle sizes. However, no biomonitoring study has been reported so far to address the metal-induced oxidative stress using different dust fractions, particularly in occupational settings. We designed a systematic cross-sectional study involving 110 chromite mine workers stratified into loaders (n = 28), extractors (n = 47) and operators (n = 35), and controls (n = 30) to find out the association between dust-bound metal exposure and oxidative stress using urinary creatinine-adjusted metal level as a biomarker of metal exposure. Results suggested elevated urinary levels of Cr 51.34 ± 8.6 along with Pb 34.29 ± 4.39, Cd 21.1 ± 2.6, and Ni 18.98 ± 3.01µg/g creatinine in exposed (extractor group) workers. Correlating metal levels with oxidative stress revealed elevated malondialdehyde (MDA) levels of 62.28 ± 5.52nM/dl among the extractors showing high levels of lipid peroxidation. Furthermore, blood superoxide dismutase (SOD) was also found significantly correlated (P = 0.000) with urinary toxic metal levels among exposed workers. We report the association between metal exposure and oxidative stress in exposed mining workers that may give rise to workers' susceptibility towards genetic and non-genetic health implications. The current study emphasized on the need for exposure control measures in the chromite ore mining activity areas.

The effects of low-toxic herbicide Roundup and glyphosate on mitochondria.

The effects of pesticides on the health of non-target living organisms in agricultural areas are critically important aspects for their safe use. Their release into the environment is an inevitable aspect for predicting and evaluation of the risk of their application. Roundup, a glyphosate-based herbicide, has been designed as an effective pesticide against weeds and now is the most widely used agrochemicals around the world due to its highly specific action of the biosynthesis of certain amino acids in plants. Despite it is claimed to be low toxic for not-target organisms, due to its broad application Roundup and products of its degradation were detected in organisms of diverse animals and humans. In this review, we describe animal and human studies of general adverse effects of Roundup and its principal substance glyphosate with focus on endocrine disruption, oxidative stress and behavioral disorders. At mechanistic level, we focus on the potential toxicity of the herbicide Roundup and glyphosate as effectors of bioenergetic functions of mitochondria. Their effects on mitochondrial membrane potential and oxidative phosphorylation are among described to date critical components responsible for its toxicity. Finally, we discuss general molecular mechanisms potentially involved in the interaction between glyphosate and mitochondria which to some extent are associated with generation of reactive oxygen species.

Organic Nanoparticles Based on D-A-D Small Molecule: Self-Assembly, Photophysical Properties, and Synergistic Photodynamic/Photothermal Effects.

Cancer is one of the major diseases threatening human health. Traditional cancer treatments have notable side-effects as they can damage the immune system. Recently, phototherapy, as a potential strategy for clinical cancer therapy, has received wide attention due to its minimal invasiveness and high efficiency. Herein, a small organic molecule (PTA) with a D-A-D structure was prepared via a Sonogashira coupling reaction between the electron-withdrawing dibromo-perylenediimide and electron-donating 4-ethynyl-N,N-diphenylaniline. The amphiphilic organic molecule was then transformed into nanoparticles (PTA-NPs) through the self-assembling method. Upon laser irradiation at 635 nm, PTA-NPs displayed a high photothermal conversion efficiency (PCE = 43%) together with efficient reactive oxygen species (ROS) generation. The fluorescence images also indicated the production of ROS in cancer cells with PTA-NPs. In addition, the biocompatibility and photocytotoxicity of PTA-NPs were evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and live/dead cell co-staining test. Therefore, the as-prepared organic nanomaterials were demonstrated as promising nanomaterials for cancer phototherapy in the clinic.