Radical Reactive Oxygen Species Research Articles

Defect-Rich Metastable MoS2 Promotes Macrophage Reprogramming in Breast Cancer: A Clinical Perspective.

Tumor-associated macrophages (TAMs) play a crucial function in solid tumor antigen clearance and immune suppression. Notably, 2D transitional metal dichalcogenides (i.e., molybdenum disulfide (MoS2) nanozymes) with enzyme-like activity are demonstrated in animal models for cancer immunotherapy. However, in situ engineering of TAMs polarization through sufficient accumulation of free radical reactive oxygen species for immunotherapy in clinical samples remains a significant challenge. In this study, defect-rich metastable MoS2 nanozymes, i.e., 1T2H-MoS2, are designed via reduction and phase transformation in molten sodium as a guided treatment for human breast cancer. The as-prepared 1T2H-MoS2 exhibited enhanced peroxidase-like activity (≈12-fold enhancement) than that of commercial MoS2, which is attributed to the charge redistribution and electronic state induced by the abundance of S vacancies. The 1T2H-MoS2 nanozyme can function as an extracellular hydroxyl radical generator, efficiently repolarizing TAMs into the M1-like phenotype and directly killing cancer cells. Moreover, the clinical feasibility of 1T2H-MoS2 is demonstrated via ex vivo therapeutic responses in human breast cancer samples. The apoptosis rate of cancer cells is 3.4 times greater than that of cells treated with chemotherapeutic drugs (i.e., doxorubicin).

Highly Efficient Quenching of Singlet Oxygen by DNA Origami Nanostructures.

DNA origami nanostructures (DONs) are able to scavenge reactive oxygen species (ROS) and their scavenging efficiency toward ROS radicals was shown to be comparable to that of genomic DNA. Herein, we demonstrate that DONs are highly efficient singlet oxygen quenchers outperforming double-stranded (ds) DNA by several orders of magnitude. To this end, a ROS mixture rich in singlet oxygen is generated by light irradiation of the photosensitizer methylene blue and its cytotoxic effect on Escherichia coli cells is quantified in the presence and absence of DONs. DONs are found to be vastly superior to dsDNA in protecting the bacteria from ROS-induced damage and even surpass established ROS scavengers. At a concentration of 15 nM, DONs are about 50000 times more efficient ROS scavengers than dsDNA at an equivalent concentration. This is attributed to the dominant role of singlet oxygen, which has a long diffusion length and reacts specifically with guanine. The dense packing of the available guanines into the small volume of the DON increases the overall quenching probability compared to a linear dsDNA with the same number of base pairs. DONs thus have great potential to alleviate oxidative stress caused by singlet oxygen in diverse therapeutic settings.

Defect-mediated time-efficient photocatalytic degradation of methylene blue and ciprofloxacin using tungsten-incorporated ternary perovskite BaSnO3 nanoparticles

Photocatalytic water purification has been extensively explored for its economic, eco-friendly, and sustainable aspects. In this study, tungsten (W) incorporated BaSn1-xWxO3 (x = 0 to 0.05) nanoparticles synthesized by facile hydrogen peroxide precipitation route has been demonstrated for photocatalytic degradation of methylene blue (MB) dye and ciprofloxacin (CIP) antibiotic. The structural analysis indicates the presence of hybrid composite-like nanostructures with reduced crystallinity. Optical studies reveal blueshift in bandgap and decrease in oxygen vacancy defects upon W-incorporation. Pure BaSnO3 shows overall enhanced photocatalytic activity towards MB (90.22%) and CIP (78.12%) after 240 min of white LED light and sunlight irradiation respectively. The 2 % W-incorporated BaSnO3 shows superior photocatalytic degradation of MB (26.89%) and CIP (45.14%) within first 30 min of irradiation confirming the presence of W to be beneficial in the process. The free radical study revealed the dominant role of reactive hole (h+) and oxygen radical (O2•−) species during photodegradation and their intermediates are investigated to elucidate the degradation mechanism of MB within 30 min of irradiation. This study is promising towards developing defect mediated and time-efficient photocatalysts for environmental remediation.

PENGARUH PEMBERIAN EKSTRAK DAUN BELALAI GAJAH TERHADAP KADAR MALONDIALDEHID DAN SUPEROKSIDA DISMUTASE PADA TIKUS DENGAN AKTIVITAS TINGGI

Clinacanthus nutans Lindau is known as the elephant trunk leaf which belongs to the Acanthaceae family. C. nutans can act as an antioxidant by reducing free radicals from the mitochondrial electron transport chain in the cell membrane. In this study, elephant trunk leaves will be studied regarding their content and antioxidant activity and their association with free radicals/Reactive Oxygen Species (ROS), which are compounds that are highly reactive. ROS can cause damage to cell integrity and functional cell disruption. Free radical reduction prevents lipid oxidation, which then reduces malondialdehyde (MDA) levels. By potentiating the antioxidant properties of Superoxide Dismutase (SOD) and reducing lipid peroxidation, C. nutans can reduce oxidative stress. The purpose of this study was to evaluate the effect of elephant trunk leaf extract on malondialdehyde and superoxide dismutase levels in rats with high activity. The research method used was laboratory experimental research with a Randomized Posttest Only with Control Group Design. In this study, 25 male white rats of the Wistar strain were divided into 5 groups: normal, negative control, and treatment I, II, III which were given elephant trunk leaf extract at successive doses of 50, 300, and 2000 mg/kg BW ( Weight). and high activity for 14 days. MDA measurements using a spectrophotometer and SOD using calorimetry were carried out after 14 days. The results showed that elephant trunk leaf extract reduced MDA levels and increased SOD activity in the blood plasma of rats induced by high activity (P value <0.05).

Controllable Photocleavage of Blebbistatin Derivatives as Photoremovable Protecting Groups.

Blebbistatin was demonstrated as a promising two-photon near-infrared activated photoremovable protecting group of hydroxyl radicals with various potential applications. However, the photocleavage mechanism of the blebbistatin derivatives remains ambiguous. Herein, blebbistatin derivatives with various electronic characteristic leaving groups were synthesized and studied, and the photocleavage mechanism(s) and the tunable effect of the leaving groups were unveiled by combining photoproduct analysis, reactive oxygen radical species detection, femtosecond transient absorption spectroscopy, and density functional theory calculation. More substantial electron-withdrawing leaving groups facilitate heterolysis of the C-O bond, which results in a cationic intermediate and a corresponding remnant. Weaker electron-withdrawing groups lead to a higher proportion of homolysis of the C-O bond, accompanied by the generation of the reactive oxygen radical species. With this structure-property relationship, the protected groups of the molecules of interest can be rationally chosen to satisfy the different requirements needed for specific applications.

Chirality‐Dependent Reprogramming of Macrophages by Chiral Nanozymes

AbstractIt is known that extracellular free radical reactive oxygen species (ROS) rather than intracellular ROS plays a non‐substitutable role in regulation of tumor‐suppressing (M1) tumor‐associated macrophages (TAMs) polarization. However, most therapeutic nanoplatforms mainly provide intracellular ROS and exhibit insufficient accumulation near TAMs, which strongly limits the macrophage‐based immunotherapeutic effects. Here we design and synthesize chiral MoS2/CoS2 nanozymes with peroxidase (POD)‐like and catalase (CAT)‐like activities to efficiently modulate TAMs polarization and reverse tumor immunosuppression by harnessing their chirality‐specific interactions with biological systems. MoS2/CoS2 nanoparticles coordinated with d‐chirality (d‐NPs, right‐handed) show improved pharmacokinetics with longer circulating half‐life and higher tumor accumulation compared with their l (left‐handed)‐ and dl (racemate)‐counterparts. Further, d‐NPs can escape from macrophage uptake in the tumor microenvironment (TME) with the aid of cell‐unpreferred opposite chirality and act as extracellular hydroxyl radicals (⋅OH) and oxygen (O2) generators to efficiently repolarize TAMs into M1 phenotype. On the contrary, l‐NPs showed high cellular uptake due to chirality‐driven homologous adhesion between l‐NPs and macrophage membrane, leading to limited M1 polarization performance. As the first example for developing chiral nanozymes as extracellular‐localized ROS generators to reprogram TAMs for cancer immunotherapy, this study opens an avenue for applications of chiral nanozymes in immunomodulation.

Chirality-Dependent Reprogramming of Macrophages by Chiral Nanozymes.

It is known that extracellular free radical reactive oxygen species (ROS) rather than intracellular ROS plays a non-substitutable role in regulation of tumor-suppressing (M1) tumor-associated macrophages (TAMs) polarization. However, most therapeutic nanoplatforms mainly provide intracellular ROS and exhibit insufficient accumulation near TAMs, which strongly limits the macrophage-based immunotherapeutic effects. Here we design and synthesize chiral MoS2 /CoS2 nanozymes with peroxidase (POD)-like and catalase (CAT)-like activities to efficiently modulate TAMs polarization and reverse tumor immunosuppression by harnessing their chirality-specific interactions with biological systems. MoS2 /CoS2 nanoparticles coordinated with d-chirality (d-NPs, right-handed) show improved pharmacokinetics with longer circulating half-life and higher tumor accumulation compared with their l (left-handed)- and dl (racemate)-counterparts. Further, d-NPs can escape from macrophage uptake in the tumor microenvironment (TME) with the aid of cell-unpreferred opposite chirality and act as extracellular hydroxyl radicals (⋅OH) and oxygen (O2 ) generators to efficiently repolarize TAMs into M1 phenotype. On the contrary, l-NPs showed high cellular uptake due to chirality-driven homologous adhesion between l-NPs and macrophage membrane, leading to limited M1 polarization performance. As the first example for developing chiral nanozymes as extracellular-localized ROS generators to reprogram TAMs for cancer immunotherapy, this study opens an avenue for applications of chiral nanozymes in immunomodulation.

Benefits of Natural Antioxidants on Oral Health.

In recent years, special attention has been paid to the correlation between oxidation-reduction mechanisms and human health. The free radicals produced via physiological cellular biochemical processes are major contributors to oxidation phenomena. Their instability is the major cause of cellular damage. Free radical reactive oxygen species containing oxygen are the best-known ones. The body neutralises the harmful effects of free radicals via the production of endogenous antioxidants (superoxide dismutase, catalase, glutathione, and melatonin). The field of study of nutraucetics has found antioxidant capacity in substances such as vitamins A, B, C, E, coenzyme Q-10, selenium, flavonoids, lipoic acid, carotenoids, and lycopene contained in some foods. There are several areas of investigation that aim to research the interaction between reactive oxygen species, exogenous antioxidants, and the microbiota to promote increased protection via the peroxidation of macromolecules (proteins, and lipids) by maintaining a dynamic balance among the species that make up the microbiota. In this scoping review, we aim to map the scientific literature on oxidative stress related to the oral microbiota, and the use of natural antioxidants to counteract it, to assess the volume, nature, characteristics, and type of studies available to date, and to suggest the possible gaps that will emerge from the analysis.

Therapeutic effects of atorvastatin on doxorubicin-induced hepatotoxicity in rats via antioxidative damage, anti-inflammatory, and anti-lipotoxicity.

Doxorubicin (DOX), is a high efficiency anthracycline antitumor drug. However, the clinical application of DOX is limited mainly by dose-related adverse drug reactions. Currently, the therapeutic effects of Atorvastatin (ATO) on DOX-induced hepatotoxicity were studied in vivo. The results indicated that DOX impaired hepatic function, as measured by an increased levels of liver weight index and serum concentrations of aspartate transaminase and alanine transaminase, as well as alteration of hepatic histology. In addition, DOX increased the serum levles of triglyceride(TG) and nonestesterified fatty acid. ATO prevented these changes. Mechanical analysis revealed that ATO restored the changes of malondialdehyde, reactive oxygen radical species, glutathione peroxidase and manganese superoxide dismutase. Additionally, ATO inhibited the increased expression levels of nuclear factor-kappa B and interleukin 1β, hence suppressing inflammation. Meanwhile, ATO inhibited cell apoptosis by dramatically decreasing the Bax/Bcl-2 ratio. In addition, ATO mitigated the lipidtoxicity by inhibiting the adipolysis of TG and accelerating hepatic lipid metabolism. Taken together, the results suggest ATO has therapeutic effect on DOX-induced hepatotoxicity via inhibition of oxidative damage, inflammatory and apoptosis. In addition, ATO attenuates DOX-induced hyperlipidemia via modulation of lipid metabolism.

A chemical timer approach to delayed chemiluminescence

Although the onset time of chemical reactions can be manipulated by mechanical, electrical, and optical methods, its chemical control remains highly challenging. Herein, we report a chemical timer approach for manipulating the emission onset time of chemiluminescence (CL) reactions. A mixture of Mn2+, NaHCO3, and a luminol analog with H2O2 produced reactive oxygen species (ROS) radicals and other superoxo species (superoxide containing complex) with high efficiency, accompanied by strong and immediate CL emission. Surprisingly, the addition of thiourea postponed CL emission in a concentration-dependent manner. The delay was attributed to a slow-generation-scavenging mechanism, which was found to be generally applicable not only to various types of CL reagents and ROS radical scavengers but also to popular chromogenic reactions. The precise regulation of CL kinetics was further utilized in dynamic chemical coding with improved coding density and security. This approach provides a powerful platform for engineering chemical reaction kinetics using chemical timers, which is of application potential in bioassays, biosensors, CL microscopic imaging, microchips, array chips, and informatics.

Engineering dual catalytic nanomedicine for autophagy-augmented and ferroptosis-involved cancer nanotherapy

Chemodynamic therapy represents a distinct anti-tumor strategy by activating intratumoral chemical catalytic reactions to produce highly toxic reactive oxygen species (ROS) from non-/limited-toxic nanocatalysts. However, the low efficacy of ROS generation still remains a major challenge for further clinical translation. Herein, a liposomal nanosystem which simultaneously encapsulated copper peroxide nanodots (CPNs) and artemisinin (ART) was constructed for autophagy-enhanced and ferroptosis-involved cancer cell death owing to Cu-based dual catalytic strategy. To be specific, the CPN components, served as a H2O2 self-supplying platform, release H2O2 and Cu2+ under acidic tumor environment and endogenously generate .OH via Fenton-like reaction (catalytic reaction I). In addition, Cu2+ species catalyze ART components to produce ROS radicals (catalytic reaction II), further augmenting the intracellular oxidative damage and lipid peroxide accumulation, leading to cancer cell death. Specifically, ART also acted as a potent autophagy inducer increasing the level of intracellular iron pool through degradation of ferritin, which could promote cancer cell ferroptosis, producing the best antineoplastic effect. After accumulation into the tumor sites, ultrasound irradiation was applied to trigger the release of CPNs and ART from liposomal nanosystems, and amplify the efficacy of catalytic reaction for maximum therapeutic effect. Both in vitro and in vivo therapeutic outcomes suggest the outstanding autophagy-augmented ferroptosis-involved cancer-therapeutic efficacy, which was further corroborated by transcriptome sequencing. In this work, Cu was firstly proven to trigger ART to produce ROS species, but also provide a TME-responsive nanoplatform for potentially suppressing tumor growth by autophagy-augmented ferroptosis-involved cancer nanotherapy.

Mitochondria/RNA cascade-targeted and fluorescence-switchable photosensitizer for photodynamic therapy augmentation and real-time efficacy self-monitoring

The localization of photosensitizers and timely efficacy evaluation highly affect efficiency of photodynamic therapy (PDT) and the resistance of residual tumor cells. Mitochondria-targeted PDT is an effective modality; however, it may encounter certain resistance caused by autophagy, a cytoprotective manner competing with cell apoptosis. Mitochondria and RNA interact closely in cell apoptosis and autophagy processes. Here, a multifunctional photosensitizer (M1) is developed for cascade mitochondria- and RNA-targeted PDT and efficacy self-monitoring. It possesses the capabilities of radical reactive oxygen species generation and migration from mitochondria to RNA in cells accompanied by fluorescence turn-on during PDT. The subsequent RNA targeting by M1 can suppress autophagy and promote mitochondria-mediated cell apoptosis. Moreover, with RNA-specific switch-on and photostable fluorescence, M1 can also be used for real-time monitoring therapeutic responses of PDT. Our study provides insights into the mechanism and regulation of cell apoptosis, autophagy, and PDT resistance by a cascade-binding photosensitizer, inspiring the design of multi-targeted and fluorescence-switchable single-molecule photosensitizers.

Abstract 123: Reactive oxygen species (ROS) as mediators of the cancer cell’s transition into the polyaneuploid cancer cell (PACC) state

Abstract Metastatic cancer is lethal and incurable due to the emergence of therapeutic resistance, resulting in the deaths of 10 million people each year. Our data suggests that therapeutic resistance is mediated by stress-induced transition into a protective polyaneuploid cancer cell (PACC) state. The PACC state is characterized by large size, polyploidization of the original aneuploid genome, and pause in cell cycle. Once released from stress, some PACCs survive to repopulate a non-polyploid, resistant cancer cell population. Using Nanostring technology to profile cisplatin-induced PACCs in prostate cancer PC3 and breast cancer MDA-MB-231 cells, we observed significant increase in gene expression related to reactive oxygen species (ROS) and the DNA damage response (DDR). We hypothesize that ROS mediate a cancer cell’s ability to enter the PACC state to survive chemotherapy.ROS are produced as byproducts of cellular respiration and are present in all cells. ROS radicals are damaging to cellular macromolecules, particularly DNA. Cancer cells have evolved to withstand high ROS, but the increase in radicals contribute to genomic instability. ROS-induced DNA damage activates the DDR leading to four possible fates: continued cycling, DNA repair, apoptosis, or cell cycle arrest. Therapy significantly increases DNA damage while also increasing total ROS levels. At this level of DNA damage, the likely cell fates are death or cycle arrest. We induced the PACC state in PC3 cells with cisplatin and monitored ROS during PACC formation (24, 48, and 72 hours) using fluorescent microscopy and flow cytometry techniques. After 72 hours, the only surviving cells are in the PACC state. We found a step wise increase in the amount of ROS per cell across treatment time. By 72 hours, total ROS is 7-fold higher in PACCs compared to the parental control. PACCs are substantially larger than parental controls, so cell size must be considered. After adjusting for unit area, we found treated cells have a higher level of ROS compared to parental cells. The greatest increase in ROS per area was seen at 24hrs, suggesting there is an initial spike in ROS at the introduction of therapy. This suggests that the ability to enter the PACC state may be due to cell cycle arrest as a response to the extensive ROS caused by therapy. To assess cells that survive therapy in the PACC stateand produce resistant progeny, we induced PACC formation, then released therapy and monitored ROS for 10 days. Adjusted for area, ROS levels remained stable and elevated compared to parental control for 10 days following therapy release. The increase in ROS per unit area shows high ROS is not simply due to increased size. The stability over time suggests PACCs are able to manage ROS levels to prevent death by oxidative stress. Future work will evaluate PACCs induced by non-platinum chemotherapies, as well as, in additional cell lines. Citation Format: Morgan D. Kuczler, Kenneth J. Pienta, Sarah R. Amend. Reactive oxygen species (ROS) as mediators of the cancer cell’s transition into the polyaneuploid cancer cell (PACC) state [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 123.

Histopathological study of the effect of glutathione in decreasing pathological changes induced by estrogen in internal organs of albino mice

In recent years, there has been a great deal of attention toward the field of free radical chemistry. Free radicals reactive oxygen species and reactive nitrogen species are generated by our body by various endogenous systems, exposure to different physiochemical conditions or pathological states. A balance between free radicals and antioxidants is necessary for proper physiological function. If free radicals overwhelm the body’s ability to regulate them, a condition known as oxidative stress ensues. Free radicals thus adversely alter lipids, proteins, and DNA and trigger a number of human diseases. This study was designed to determine the influence of Glutathione to reduce the pathological changes induced by estrogen. In this study 40 female and male mice are taken at age of 21days with groups of control (10 mouse in each group).The group of experimental animals was treated with estrogen and glutathione diluted with distilled water, as a vehicle, and injected intraperitonially for 12 weeks, once weekly. Each control group was injected with the vehicle of it in the same manner of injection and for the same period.

Electron localization of ZnO/Znln2S4 interface induced lattice relaxation for triggering photocatalytic uranium evolution

Designing a material that efficiently extracts uranium (U) from natural seawater and resists biofouling remains a critical challenge. Here, flake Znln2S4 grew in situ on the surface of black porous zinc oxide (B-ZnO), and finally a binary composite material (B-ZnO/ZnIn2S4) is synthesized. Based on the reduction process of U(VI), the chemical reaction of the U(VI) → U(IV) process occurred on the surface and interface of the composite material. The S-scheme heterojunction system constructed of ZnO and Znln2S4 with a matching band structure showed great potential for promoting the separation and transfer of photogenerated carriers and obtaining powerful photoredox capabilities. By generating biologically toxic free radical reactive oxygen species and Zn2+, the adsorbent had high antibiological fouling activity. After 120 min of extraction in simulated seawater, the light-induced reduction ability of B-ZnO/ZnIn2S4-45% (mass ratio) on U(VI) reached 99%, which was 6.2 times higher than that under dark conditions. The conversion path of U(VI) was calculated by density functional theory (DFT). In addition, ZnIn2S4 (007) exhibited the ability to localize to the surface of ZnO (002) and promote electron transfer. These results indicate that interface atomic structure engineering is crucial for the synthesis of efficient and durable seawater U(VI) extraction catalysts.

An overview of free Radicals & antioxidants and its Deletenous actions.

In modern years, there has been a large dealing of work toward the area of free radical chemistry. Free radicals reactive oxygen species and reactive nitrogen species are create by our body by various endogenic systems, influence to different physio chemical conditions or unhealthy states. A balance between free radicals and antioxidants is necessary for proper physiological function. If free radicals overwhelm the body's ability to modulate them, a condition known as oxidative stress ensues. Free radicals thus unfavorable alter lipids, proteins, and DNA and activate a number of human diseases. Hence application of external source of antioxidants can assist in coping this oxidative stress. Synthetic antioxidants such as butylated hydroxytoluene and butylated hydroxyanisole have recently been reported to be dangerous for human health. The present review provides a brief overview on oxidative stress mediate cellular damages and role of dietary antioxidants as functional foods in the organization of human diseases. We need to take balance diet which provide much more antioxidants to lower risks of health and run to life longer.The purpose of this review is that we want awareness related to sources of antioxidants from plants and highlight the studies of antioxidants and free radicals which provide prove for maintaining healthy aging.
 Key words: antioxidant, free radicals, aging, oxidative stress.
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Antiphotoaging properties of Zingiber montanum essential oil isolated by solvent-free microwave extraction against ultraviolet B-irradiated human dermal fibroblasts.

Maintaining youthful skin from photoaging with natural products, including essential oils, is a vital strategy that has piqued the interest of researchers in the pharmaceutical and cosmetic industries. This research aimed to investigate the protective properties of Zingiber montanum (J. Koenig) Link ex A. Dietr. essential oil against ultraviolet B (UVB)-induced skin damage and photoaging in normal human dermal fibroblast (HDFn) cells. The essential oil was extracted from fresh plant rhizomes using solvent-free microwave extraction. Its antiphotoaging properties in HDFn cells were investigated using reactive oxygen species (ROS)-scavenging, wound healing, matrix metalloproteinases (MMP-1, MMP-3, and MMP-9) expression, procollagen synthesis, and elastase and tyrosinase inhibitory assays. The results showed that the test oil exhibited no significant toxicity in HDFn at concentrations up to 10mg/mL, with cell viability exceeding 90%. Following UVB irradiation at 30mJ/cm2, Z. montanum oil demonstrated time and concentration-dependent ROS radical scavenging capabilities. In a cell migration assay, the essential oil demonstrated wound-healing properties. Z. montanum oil suppressed the expression of MMPs and enhanced the synthesis of type I procollagen at a concentration of 0.1-1mg/mL. In addition, 0.1-1mg/mL Z. montanum oil inhibited elastase activity in a concentration-dependent manner but did not affect tyrosinase activity. From these findings, the essential oil of Z. montanum could have potential applications in developing cosmeceutical products to prevent skin photoaging.

Type I AIE photosensitizers: Mechanism and application

AbstractPhotodynamic therapy (PDT) with plenty of advantages is expected to become a promising modality for cancer treatment, but challenges still remain. In the past decade, abundant photosensitizers (PSs) with aggregation‐induced emission (AIE) property make the development of PSs enter upon a new phase, offering incomparable merits. Recently, Type I AIE PSs with capability of generating radical reactive oxygen species (ROS) have emerged as strong candidates to overcome the inherent hypoxia nature of solid tumors. In this review, detailed discussions on the mechanisms of PDT are drawn to highlight the basic advantages of Type I pathway over Type II one in hypoxic PDT, followed by a summary of frequently‐used detection methods for the accurate distinguishing of the nature of ROS. Finally, the latest representative advances are summarized, and future perspectives of Type I AIE PSs are discussed.

Oxidative stress in leukemia and antioxidant treatment.

Oxidative stress is caused by the imbalance between the generation of free radicals/reactive oxygen species (ROS) and the antioxidant defense systems, which can activate various transcription factors and affect their transcriptional pathways. Oxidative stress plays an important role in the occurrence and development of leukemia and is closely related to the treatment and prognosis of leukemia. The standard chemotherapy strategies for the pre-treatment of leukemia have many drawbacks. Hence, the usage of antioxidants and oxidants in the treatment of leukemia is being explored and has been preliminarily applied. This article reviews the research progress of oxidative stress and leukemia. In addition, the application of antioxidants treatment in leukemia has been summarized.

Cisplatin-induced neurotoxicity in cerebellar cortex of male mice involves oxidative stress and histopathology

BackgroundDespite evidence of neurotoxicity, cisplatin is still considered the most potent drug prescribed in human chemotherapy for a broad spectrum of malignancies. The objective was to evaluate the cerebellar cortex damage including oxidative stress biomarkers and histopathology aspects in male mice. One saline control group and two cisplatin groups were intraperitoneally injected with 0, 5, and 10 mg/kg body weight (bw) cisplatin, twice per week for four successive weeks, respectively.ResultsCisplatin decreased the body weights of treated mice. Serum levels of superoxide dismutase and glutathione peroxidase were significantly reduced in the 5 and 10 mg/kg dose, twice weekly for 4 weeks treatment; in contrast, there was a significant increase of lipid peroxidation. 5 and 10 mg/kg bw of cisplatin caused histopathological damage in the cerebellum tissue characterized by disruption, disorganization, and degeneration with dense pyknotic nuclei of the granular cells. Ultrastructurally, in the cortical region of the cerebellum, the Purkinje cells showed irregular pyknotic nuclei with indistinct nucleoli, cytoplasmic vacuolation, marked indentation of the nuclear membrane, dilatation of the endoplasmic reticulum, and breakdown and disappearance of mitochondrial cristae. Moreover, the molecular layer showed cellular necrosis and an increased number of lysosomal particles. The myelinated nerve fibers showed degenerative areas distinct by splitting, disruption, and loss of the lamellar pattern of the myelin sheath.ConclusionThese findings provide a confirmed foresight that the in vivo potential treatment of mice with cisplatin induces cerebellum deficits and impairment in neuronal histology. The identified mechanism which evokes neurotoxicity is oxidative stress-dependent status. This mechanism is pharmacologically boosted by great production of free radical reactive oxygen species.