Toxic Free Radicals Research Articles

Molecular Self-Assembly of Bioorthogonal Aptamer-Prodrug Conjugate Micelles for Hydrogen Peroxide and pH-Independent Cancer Chemodynamic Therapy.

Chemodynamic therapy (CDT) has demonstrated new possibilities for selective and logical cancer intervention by specific manipulation of dysregulated tumorous free radical homeostasis. Current CDT methods largely rely on conversion of endogenous hydrogen peroxide (H2O2) into highly toxic hydroxyl radicals via classical Fenton or Haber-Weiss chemistry. However, their anticancer efficacies are greatly limited by the requirement of strong acidity for efficient chemical reactions, insufficient tumorous H2O2, and upregulated antioxidant defense to counteract free radical-caused oxidative damage. Here, we present a new concept whereby bioorthogonal chemistry and prodrug are combined to create a new type of aptamer drug conjugate (ApDC): aptamer-prodrug conjugate (ApPdC) micelle for improved and cancer-targeted CDT. The hydrophobic prodrug bases can not only promote self-assembly of aptamers but also act as free radical generators via bioorthogonal chemistry. In depth mechanistic studies reveal that, unlike traditional CDT systems, ApPdC micelles enable in situ activation and self-cycling generation of toxic C-centered free radicals in cancer cells through cascading bioorthogonal reactions, with no dependence on either H2O2 or pH, yet concurrently with diminished cancerous antioxidation by GSH depletion for a synergistic CDT effect. We expect this work to provide new insights into the design of targeted cancer therapies and studies of free radical-related molecular mechanisms.

Safer-by-design flame-sprayed silicon dioxide nanoparticles: the role of silanol content on ROS generation, surface activity and cytotoxicity

BackgroundAmorphous silica nanoparticles (SiO2 NPs) have been regarded as relatively benign nanomaterials, however, this widely held opinion has been questioned in recent years by several reports on in vitro and in vivo toxicity. Surface chemistry, more specifically the surface silanol content, has been identified as an important toxicity modulator for SiO2 NPs. Here, quantitative relationships between the silanol content on SiO2 NPs, free radical generation and toxicity have been identified, with the purpose of synthesizing safer-by-design fumed silica nanoparticles.ResultsConsistent and statistically significant trends were seen between the total silanol content, cell membrane damage, and cell viability, but not with intracellular reactive oxygen species (ROS), in the macrophages RAW264.7. SiO2 NPs with lower total silanol content exhibited larger adverse cellular effects. The SAEC epithelial cell line did not show any sign of toxicity by any of the nanoparticles. Free radical generation and surface reactivity of these nanoparticles were also influenced by the temperature of combustion and total silanol content.ConclusionSurface silanol content plays an important role in cellular toxicity and surface reactivity, although it might not be the sole factor influencing fumed silica NP toxicity. It was demonstrated that synthesis conditions for SiO2 NPs influence the type and quantity of free radicals, oxidative stress, nanoparticle interaction with the biological milieu they come in contact with, and determine the specific mechanisms of toxicity. We demonstrate here that it is possible to produce much less toxic fumed silicas by modulating the synthesis conditions.

Hyperthermia and Controllable Free Radical Coenhanced Synergistic Therapy in Hypoxia Enabled by Near-Infrared-II Light Irradiation.

Tumor cell metabolism and tumor blood vessel proliferation are distinct from normal cells. The resulting tumor microenvironment presents a characteristic of hypoxia, which greatly limits the generation of oxygen free radicals and affects the therapeutic effect of photodynamic therapy. Here, we developed an oxygen-independent free radical generated nanosystem (CuFeSe2-AIPH@BSA) with dual-peak absorption in both near-infrared (NIR) regions and utilized it for imaging-guided synergistic treatment. The special absorption provides the nanosystem with high photothermal conversion efficiency and favorably matched photoactivity in both I and II NIR biological windows. Upon NIR light irradiation, the generated heat could prompt AIPH release and decompose to produce oxygen-independent free radicals for killing cancer cells effectively. The contrastive research results show that the enhanced therapeutic efficacy of NIR-II over NIR-I is principally due to its deeper tissue penetration and higher maximum permission exposure that benefits from a longer wavelength. Hyperthermia effect and the production of toxic free radicals upon NIR-II laser illumination are extremely effective in triggering apoptosis and death of cancer cells in the tumor hypoxia microenvironment. The high biocompatibility and excellent anticancer efficiency of CuFeSe2-AIPH@BSA allow it to be an ideal oxygen-independent nanosystem for imaging-guided and NIR-II-mediated synergistic therapy via systemic administration.

Natural products and their active principles used in the treatment of neurodegenerative diseases: a review

Free radicals are the byproducts of physiological aerobic cellular metabolism. Intrinsic antioxidant system plays its pivotal function in prevention of any loss due to free radicals. Though, incorporation or excess production of free radicals from environment to living system or imbalanced defense mechanism of antioxidant system leads to severe consequences like neuro-degeneration. Sensory or functional loss occurs in neural cells in neurodegenerative diseases. Besides numerous other genetic or environmental factors, oxidative stress is the major cause which leads to damage of neurons and production of neurodegenative diseases. However, oxygen is vital for existence, excessive reactive oxygen species production and imbalanced metabolism leads to a variety of diseases such as aging, Parkinson’s disease, Alzheimer’s disease, and many other neurodegenative diseases. Free radicals toxicity contributes to DNA and proteins damage, tissue damage, inflammation and consequent cellular apoptosis. Neuroprotection is a broad term commonly used to refer therapeutic strategies that can prevent, delay or even reverse neuronal damage. Since thousands of years, lots of medicinal plants have been used in a group of herbal preparations of Ayurveda (Indian traditional health care system) named Rasayana because of the antioxidant principles present in it, responsible for their medicinal use in neurodegenerative diseases. This work constitutes a literature review on natural products contain antioxidant principles used in the treatment of neurodegenerative disease.

Therapeutic Perspective of Vitamin C and Its Derivatives.

l-Ascorbic acid (ASA), vitamin C, is a ubiquitous carbohydrate-like compound that has an essential role in a number of cellular processes, such as collagen synthesis, cellular oxidation, and various hydroxylation reactions. ASA is a biomolecule of critical importance for protection of cellular components against oxidative damage caused by toxic free radicals and other reactive oxygen species (ROS) that are involved in the development of various types of chronic diseases. Vitamin C has a switchover role from being an antioxidant in physiological conditions to a prooxidant under pathologic conditions. Moreover, some l-ascorbic acid derivatives exhibit strong and selective antitumor and antiviral activity. This review emphasizes the advances on diverse and potent biological profiles of l-ascorbic acid and its derivatives, and their perspective in the development of new bioactive chemical entities in the future. The work is primarily addressed at antioxidant, anticancer, and antiviral potencies of l-ascorbic acid and compounds containing its butenolide structural motif.

Neutrophil elastase plays a non-redundant role in remodeling the venular basement membrane and neutrophil diapedesis post-ischemia/reperfusion injury.

Ischemia/reperfusion (I/R) injury is a severe inflammatory insult associated with numerous pathologies, such as myocardial infarction, stroke and acute kidney injury. I/R injury is characterized by a rapid influx of activated neutrophils secreting toxic free radical species and degrading enzymes that can irreversibly damage the tissue, thus impairing organ functions. Significant efforts have been invested in identifying therapeutic targets to suppress neutrophil recruitment and activation post‐I/R injury. In this context, pharmacological targeting of neutrophil elastase (NE) has shown promising anti‐inflammatory efficacy in a number of experimental and clinical settings of I/R injury and is considered a plausible clinical strategy for organ care. However, the mechanisms of action of NE, and hence its inhibitors, in this process are not fully understood. Here we conducted a comprehensive analysis of the impact of NE genetic deletion on neutrophil infiltration in four murine models of I/R injury as induced in the heart, kidneys, intestine and cremaster muscle. In all models, neutrophil migration into ischemic regions was significantly suppressed in NE−/− mice as compared with wild‐type controls. Analysis of inflamed cremaster muscle and mesenteric microvessels by intravital and confocal microscopy revealed a selective entrapment of neutrophils within venular walls, most notably at the level of the venular basement membrane (BM) following NE deletion/pharmacological blockade. This effect was associated with the suppression of NE‐mediated remodeling of the low matrix protein expressing regions within the venular BM used by transmigrating neutrophils as exit portals. Furthermore, whilst NE deficiency led to reduced neutrophil activation and vascular leakage, levels of monocytes and prohealing M2 macrophages were reduced in tissues of NE−/− mice subjected to I/R. Collectively our results identify a vital and non‐redundant role for NE in supporting neutrophil breaching of the venular BM post‐I/R injury but also suggest a protective role for NE in promoting tissue repair. © 2019 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

Re‐visiting the Antioxidant Activity of Se‐ and Te‐ Carbohydrates: A Theoretical Study

AbstractAntioxidants have attracted interest for a very long time. Because of their unique ability to quench other toxic free radicals in the body, these molecules have been the focus of many chemists. Herein, we have undertaken a quantum chemical study on some carbohydrates and their heavier Se and Te derivatives to evaluate the essential parameters responsible for showing antioxidant abilities through different mechanistic pathways. The effect of different solvent media on their antioxidant ability has also been explored. Our study reveals that heavier Se and Te containing carbohydrates show higher antioxidant abilities and in addition, the aromatic derivatives of these molecules show even superior ability.

Eradication of Helicobacter pylori through the inhibition of urease and peptide deformylase: Computational and biological studies

This work tested anti- Helicobacter pylori, free radicals scavenging and toxicity property as well as chemical constituents in the extract of chloroform (CE) and ethyl acetate (EAE) from the pedicel of Diospyros kaki L. (PDK-CE and PDK-EAE). There were 33 and 36 chemical constituents respectively in the extracts of PDK-CE and PDK-EAE, belonging to the fatty acids methyl ester, fatty acids, and stearic acids, as revealed by Gas Chromatography-Mass Spectrometry (GC-MS). The extracts did not exhibit any toxicity on NIH3T3 cells, but they significantly showed scavenging of NO, DPPH, and H2O2 free radicals. The extracts displayed in vitro anti-H. pylori activity. PDK-CE had the maximum inhibitory zone at a minimal inhibitory concentration (MIC) of 10 μg. ml−1 and the extract also triggered the cellular damage in the bacteria. PDK-CE extract had a high urease inhibitory activity (IC50 value of 8.5 μg). Further, in silico studies was performed by using 41 compounds against H. pylori urease (HPU) and H. pylori peptide deformylase (HPPD). The score value was the maximum (−19.58 kcal/mol) against HPU with 17-(5-ethyl-6-methylheptan-2-yl)-10,13-dimethyl-2,3,4,7,8,9,11,12,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol, while the score value was the maximum (−14.51 kcal/mol) against HPPD with hexadecanoic acid. The results demonstrated the importance of the pedicel extracts in future pharmaceutical drug development against H. pylori infections.

Mitochondria Inspire a Lifestyle.

Tucked inside our cells, we animals (and plants, and fungi) carry mitochondria, minuscule descendants of bacteria that invaded our common ancestor 2 billion years ago. This unplanned breakthrough endowed our ancestors with a convenient, portable source of energy, enabling them to progress towards more ambitious forms of life. Mitochondria still manufacture most of our energy; we have evolved to invest it to grow and produce offspring, and to last long enough to make it all happen. Yet because the continuous generation of energy is inevitably linked to that of toxic free radicals, mitochondria give us life and give us death. Stripping away clutter and minutiae, here we present a big-picture perspective of how mitochondria work, how they are passed on virtually only by mothers, and how they shape the lifestyles of species and individuals. We discuss why restricting food prolongs lifespan, why reproducing shortens it, and why moving about protects us from free radicals despite increasing their production. We show that our immune cells use special mitochondria to keep control over our gut microbes. And we lay out how the fabrication of energy and free radicals sets the internal clocks that command our everyday rhythms-waking, eating, sleeping. Mitochondria run the show.

Vitamin E As an Antioxidant Reduces Apoptosis of Cells in Rat Hippocampus Following Exposure to Polyvinyl Chloride

Background: Many studies have shown that polyvinyl chloride (PVC) has toxic effects on the body and brain. Vitamin E is a nutritional supplement that acts as an antioxidant, scavenging toxic free radicals. Objectives: The aim of this study was to examine the protective effects of vitamin E against PVC-induced damages in rat hippocampus. Methods: In this study, 24 male Wistar rats were randomly divided to four groups (n = 6), including control, vitamin E (150 mg/kg.bw/day), PVC (1000 mg/kg.bw/day), PVC + vitamin E. The administration routes were oral and the experiment period was 40 days. At the end of the examination, rats were euthanized and the brain was removed and the left hippocampus was transferred to 10% formalin for H-E staining, TUNNEL, and crystal violet. Data were analyzed by SPSS 24 software and Tukey’s test. Results: The present results showed that oral administration of PVC was associated with an increase in apoptosis in the hippocampus. vitamin E led to suppression of apoptosis in the hippocampus of rats. Conclusions: Exposure to PVC can cause hippocampus damage, while vitamin E, as an antioxidant, may reduce the destructive effects of PVC in rat hippocampus.

Mitigation by Aqueous Extract of Celastrus Paniculatus Seeds against Monosodium Glutamate Induced Impairments in Human Neuronal cells IMR-32

The free radicals are considered as primary culprit for many multifactorial diseases. These free radicals scavenging remains a foremost challenge in most neurological disorders, which can be subjected with least collateral damage by herbal extracts. In this study, Celastrus paniculatus (CP) seeds aqueous extract (AE) (0.25, 0.5 and 1.0 µg/ml) was used to evaluate the neuroprotective efficacy against adverse effects of monosodium glutamate (MSG) (7 mM) in neuroblastoma cell line IMR-32. Preliminary pharmacological investigations and free radical scavenging capacity were evaluated for AE. Cytotoxicity and oxidative stress were studied using MTT assay and some biochemical parameters (total protein and glutathione level as well as activity of superoxide dismutase and catalase). Moreover, genotoxicity due to free radicals was also assessed using comet assay in IMR-32 cells. Results showed presence of various phytochemicals in AE and its significant inhibition of DPPH and NO radicals. AE was not only enhancing the activity of antioxidant enzymes but also reduced the free radical mediated cytotoxicity of MSG in IMR-32 cells. The DNA damage found in neuronal cells due to free radical toxicity of MSG was reduced in presence of free radical inhibitory phytochemical present in AE. From these results it can be concluded that AE of CP seeds is an effective antioxidant agent and potent neuroprotective herb to mitigate MSG induced neuronal impairments in IMR-32 cells.

Melatonin and cancer: From the promotion of genomic stability to use in cancer treatment.

Cancer remains among the most challenging human diseases. Several lines of evidence suggest that carcinogenesis is a complex process that is initiated by DNA damage. Exposure to clastogenic agents such as heavy metals, ionizing radiation (IR), and chemotherapy drugs may cause chronic mutations in the genomic material, leading to a phenomenon named genomic instability. Evidence suggests that genomic instability is responsible for cancer incidence after exposure to carcinogenic agents, and increases the risk of secondary cancers following treatment with radiotherapy or chemotherapy. Melatonin as the main product of the pineal gland is a promising hormone for preventing cancer and improving cancer treatment. Melatonin can directly neutralize toxic free radicals more efficiently compared with other classical antioxidants. In addition, melatonin is able to regulate the reduction/oxidation (redox) system in stress conditions. Through regulation of mitochondrial nction and inhibition of pro-oxidant enzymes, melatonin suppresses chronic oxidative stress. Moreover, melatonin potently stimulates DNA damage responses that increase the tolerance of normal tissues to toxic effect of IR and may reduce the risk of genomic instability in patients who undergo radiotherapy. Through these mechanisms, melatonin attenuates several side effects of radiotherapy and chemotherapy. Interestingly, melatonin has shown some synergistic properties with IR and chemotherapy, which is distinct from classical antioxidants that are mainly used for the alleviation of adverse events of radiotherapy and chemotherapy. In this review, we describe the anticarcinogenic effects of melatonin and also its possible application in clinical oncology.

Nitric oxide reverses drug resistance by inhibiting ATPase activity of p-glycoprotein in human multi-drug resistant cancer cells

BackgroundDevelopment of resistance to chemotherapy drugs is a significant problem in treating human malignancies in the clinic. Overexpression of drug efflux proteins, including P-170 glycoprotein (P-gp), an ATP-dependent efflux protein, is one of the main mechanisms responsible for multi-drug resistance (MDR). Because our previous studies have shown that nitric oxide (˙NO) or its related species inhibit the ATPase activities of topoisomerase II, we hypothesized that ˙NO should also inhibit the ATPase activity of P-gp and increase drug accumulation in MDR cells, causing a reversal of drug resistance. ResultsCytotoxicity and cellular accumulation studies showed that ˙NO significantly inhibited the ATPase activity of P-gp in isolated membranes and in NCI/ADR-RES tumor cells, causing an increase in drug accumulation and reversals of adriamycin and taxol resistance in the MDR cells. While ˙NO had no effects on topoisomerase II-induced, adriamycin-dependent DNA cleavage complex formation, it significantly inhibited adriamycin-induced DNA double-strand breaks. Electron spin resonance studies showed an increase in adriamycin-dependent hydroxyl radical formation in the presence of an NO-donor. ConclusionsThe reversal of drug resistance is due to inhibition of the ATPase activity by ˙NO, resulting in enhancement of the drug accumulation in the MDR cells. Furthermore, DNA damage was not responsible for this reversal of adriamycin resistance. However, formation of adriamycin-dependent toxic free radical species and subsequent cellular damage may be responsible for the increased cytotoxicity of adriamycin by ˙NO in NCI/ADR-RES cells. General significanceAppropriately designed NO donors would be ideal for the treatment of P-gp-overexpressing tumors in the clinic.

Acetaminophen-induced fulminant liver failure (clinical case presentation and a review of the literature)

Acetaminophen (AAP) is one of the most common and widely used antipyretic drugs, but its overdose is the leading cause of fulminant hepatic insufficiency in the world. Mechanisms of liver damage at the use of toxic doses of AAP are caused by the transformation of the isoform of cytochrome P450 (CYP2E1, CYP2A6) into a reactive metabolite, N-acetyl-parabenzoquinonimine (NAPQI), which plays a major role in hepatotoxicity. Another mechanism of hepatotoxicity includes the formation of peroxynitrite – a toxic free radical produced in the mitochondria, which causes oxidative damage. In addition to liver damage in case of acetaminophen poisoning, nephrotoxic effect can occur. Potential mechanisms of nephrotoxicity in overdose of AAP are presented, caused by cytochrome P450, as well as prostaglandin synthetase and enzyme N-deacetylase are described. In the clinical case described by us, the development of fulminant hepatic insufficiency against the background of acetaminophen administration led to the development of a coma along with the kidney damage, however, a stable positive dynamics, was achieved during treatment. In the catamnesis 2.5 years later, there were no signs of fibrosis or cirrhosis of the liver.

Effect of Charcoal in Cigarette Filters on Free Radicals in Mainstream Smoke.

The addition of charcoal in cigarette filters may be an effective means of reducing many toxicants from tobacco smoke. Free radicals are a highly reactive class of oxidants abundant in cigarette smoke, and here we evaluated the effectiveness of charcoal to reduce free radical delivery by comparing radical yields from commercially available cigarettes with charcoal-infused filters to those without and by examining the effects of incorporating charcoal into conventional cigarette filters on radical production. Commercial cigarettes containing charcoal filters produced 40% fewer gas-phase radicals than did regular cellulose acetate filter cigarettes when smoked using the International Organization of Standardization (ISO, p = 0.07) and Canadian Intense (CI, p < 0.01) smoking protocols. While mean-particulate-phase radicals were 25-27% lower in charcoal cigarettes, differences from noncharcoal products were not significant ( p = 0.06-0.22). When cellulose acetate cigarette filters were modified to incorporate different types and amounts of activated charcoal, reductions in gas-phase (>70%), but not particulate-phase, radicals were observed. The reductions in gas-phase radicals were similar for the three types of charcoal. Decreases in radical production were dose-responsive with increasing amounts of charcoal (25-300 mg) with as little as 25 mg of activated charcoal reducing gas-phase radicals by 41%. In all studies, charcoal had less of an effect on nicotine delivery, which was decreased 33% at the maximal amount of charcoal tested (300 mg). Overall, these results support the potential consideration of charcoal in cigarette filters as a means to reduce exposure to toxic free radicals from cigarettes and other combustible tobacco products.

An eco‐friendly molecular imprinting technique for the selective recognition and controlled release of bovine serum albumin

AbstractBACKGROUNDSynthesis of molecular imprinted polymer (MIP) by conventional methods is a tedious process due to the necessity for toxic organic solvents, chemicals and thermal activation for the free radical generation of initiators. In this study, a new MIP is synthesized using only the action of biopolymer blend cross‐linking in the presence of BSA as a template.RESULTSThe characteristics of the MIP were investigated using Fourier‐transform infrared spectroscopy, SEM, X‐ray diffraction and zeta potential analyses. The effects of cross‐linking density in imprinting efficiency, and the influence of pH and ionic strength in the loading of BSA into MIP were investigated. The adsorption isotherms of BSA onto MIP and nonimprinted polymer (NIP) were determined by a Langmuir model and showed a maximum binding capacity of 95.73 mg g−1 for MIP and 76.08 mg g−1 for NIP.CONCLUSIONThe porous structure formed in the polymer blend of MIP enables easy access of proteins by diffusion as clearly shown in an SEM image. Compared with the NIP blends, the MIP blends demonstrated much higher adsorption capacity due to the presence of multiple hydrogen bonds and covalent bond interaction between the imprinted cavities and template proteins. The merits of this novel technique include elimination of a complex polymerization reaction, toxic volatile organic solvents and free radical initiators. Thus, this new way of strategy will be a promising trend for the future preparation of environmentally benign molecular imprinted polymer materials. © 2018 Society of Chemical Industry

The ability to determine the non-transferrin-bound iron and total iron in the human placenta using high-performance liquid chromatography method

Iron is one of the most important microelements in the human body. It is a component of haemoglobin, which transports oxygen to all cells in the organism. It is also used in the synthesis of myelin, neurotrans-mitters, and DNA and transfers electrons in biochemical reactions. Iron is also responsible for regular development of the foetus’ central nervous system. Furthermore, as a result of Fenton reactions, iron leads to formation of toxic free radicals. The existence of non-transferrin-bound iron (NTBI) and its part desfer-rioxamine-chelatable iron (DCI) can be used to assess this element in the body. The placenta is an organ transition that is formed during pregnancy in the female organism. It has a dense web of blood vessels in which dynamic exchange of blood between mother and foetus takes place. As a result, a fraction of NTBI may be present in the placenta. The main goal of this work was to develop a method for determining total iron and desferrioxamine-chelatable iron in solid tissues - the human placenta.

ANTIOXIDANT MEDIATED DEFENSE ROLE OF ECLIPTAALBA HERBAL EXTRACT AGAINST CCL4 INDUCEDTOXIC HEPATITIS

Objective: The present study focuses on the antioxidant mediated protective effect of a popular medicinal herbEcliptaalba against CCl4induced oxidative stress in the liver of rats.Methods: Rats divided into four groups were administered with CCl4 andCCl4 along with methanol extract of leaves of Eclipta herb (200 and 400 mg/kg b. wt) for three weeks. At the end of treatment, rats were anaesthetized and blood samples were collected for serum separation. Biochemical analysis such as alanineaminotransferase (ALT), aspartateaminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and total bilirubin (TB) were done in serum. Liver tissue was used for glutathione (GSH), lipid peroxidation (LPO), gluatathione peroxidase (GPx), glutathione Stransferase (GST), superoxide dismutase (SOD)and catalase (CAT) analysis. CCl4 administration caused significant elevation of the serum enzymes and total bilirubin content.Results: Antioxidant enzymes were drastically inhibited with significant reduction of glutathione and increased lipid peroxidation in CCl4 treated rats. Ecliptaalbaextracts administrated rats, however did not show much changes in marker enzyme level. Antioxidant enzyme status was also not affected and found nearer to the control levels. Increased gluatathione level and reduced lipid peroxidation was also evident in Eclipta alba treated rats.Conclusion: The findings show that Eclipta alba extract offers better protection against the free radical toxicity of CCl4.

Controllable Generation of Free Radicals from Multifunctional Heat-Responsive Nanoplatform for Targeted Cancer Therapy

Targeted drug delivery and controllable generation of oxygen-independent toxic free radicals in tumor hypoxia environments are of great importance in cancer therapy. Here, a thermoresponsive nanoplatform was introduced by modifying carbon-coated iron carbide (Fe5C2) nanoparticles with bovine serum albumin (BSA) to achieve better water solubility and biocompatibility. Then a type of polymerization initiator (AIPH) was effectively loaded on the surface of Fe5C2–BSA nanoparticles and sealed by a phase change material (PCM) for higher drug loading and controlled drug release stimulated by heat. Upon illumination by near-infrared light, the photothermal effect of Fe5C2 nanoparticles melts the PCM, triggering the release of encapsulated AIPH to produce free radicals, which effectively kill the hypoxia cancer cells. Additionally, the special magnetic performance enables targeted and tracked therapy under the driving of an external magnetic field. What’s more, the as-prepared multifunctional theranostic nanoplatf...

X rays induced oxidative stress in cerebral tissue of albino wistar rats

Radiotherapy has been increasingly used as an effective tool in the treatment of cancer. Radiations might produce toxic effects to the surrounding normal cells mediated by free radicals. The study of normal tissue response to x rays is of great importance in cancer patients who undergo radiotherapy. Brain is the logical target of free radical injury due to high lipid content and low antioxidants. Hence, this study was undertaken to study the toxic effects of radiation on brain. Albino rats exposed to whole body radiation of 6 Gy per minute formed test group and rats that were not irradiated formed control group. Each group had eight animals . Malondialdehyde, SOD, catalase, glutathione and acetyl choline esterase were estimated in brain homogenates by spectrophotometric methods. Brain antioxidant enzymes viz., SOD and catalase decreased significantly in rats exposed to radiations compared to normal rats. Acetyl cholinesterase a marker of low grade inflammation increased significantly in x ray treated rats. The increase in lipid peroxidation was also statistically significant in these rats compared to control group. On the whole, it can be concluded that free radical toxicity may be one of the major factors contributing to radiation pathology in rats.