Organ Toxicity Research Articles

STUDY OF TOXICOLOGY OF THE ANTITUMOR DRUG COLCHIPRIT-NEO (K-20)

Objective: Colchiprit-neo was administered orally to rats at dosages of 30.0, 61.0, and 120 mg/kg for 30 days in order to assess its chronic toxicity. Methods: The effects on behavior, body weight, peripheral blood composition, kidney function, liver enzyme levels, and internal organ pathology were evaluated after rats were given Colchiprit-neo at the recommended dosages. To assess the reversibility of any possible harmful effects, a one-month recovery time was incorporated. Results: According to the study, rats' behavior, body weight, and blood composition were unaffected by repeated oral treatment of Colchiprit-neo. During therapy, the liver's alanine aminotransferase (ALT) level rose, but during the recovery phase, all tested values went back to normal. The 30 mg/kg dose did not cause any toxicity in the parenchymal organs, according to pathomorphological analysis. Novelty: The findings indicate that Colchiprit-neo is safe for long-term usage because it does not show substantial chronic toxicity at therapeutic levels. This work offers significant preclinical evidence in favor of its possible therapeutic use without endangering the major organ systems.

Weight loss and metabolic effects of an ALDH1A1-specific inhibitor, FSI-TN42, in a diet induced mouse model of obesity.

Retinoic acid (RA) participates in weight regulation and energy metabolism. Mice lacking ALDH1A1, one of the major enzymes responsible for RA biosynthesis, are resistant to diet-induced obesity. Previously, we identified FSI-TN42 (N42) as an ALDH1A1-specific inhibitor and reported its pharmacokinetics and pharmacodynamics as well as its efficacy in weight suppression. In the first study, C57BL/6 J male mice were fed a high fat diet for 8 weeks to induce obesity. Mice were then divided into three groups and fed (1) moderate fat diet (MFD), (2) MFD + WIN 18,446 (1 g/kg diet), or (3) MFD + N42 (1 g/kg diet) for 8 weeks. A control group of mice were fed a low-fat diet for the entire period. Mice were weighed weekly and fasting glucose was determined every 4 weeks. Tissues were examined for potential toxicity using histopathology and complete blood counts. In the second study, we examined influences of N42 on energy balance and/or appetite by determining food intake, activity and energy expenditure in mice with obesity treated with MFD or MFD + N42. Lastly, we tested fertility with a mating study. N42 significantly accelerated weight loss compared to MFD alone in mice with obesity by reducing fat mass without decreasing lean mass. N42 did not alter food intake or activity levels. While mice treated with N42 lost significantly more weight, they maintained a similar level of energy expenditure compared to mice fed MFD only. Mice fed N42 preferentially used fat postprandially, especially under thermoneutral or mild cold challenge. N42 did not affect male fertility. N42 promotes weight loss when used with MFD in mice with diet-induced obesity without causing significant organ toxicity or male infertility. Future studies will determine if N42 can be used to promote further weight loss if combined with current weight loss drugs.

Importance of sex-dependent differences for dosing selection and optimization of chemotherapeutic drugs.

Background Despite major advances in cancer treatment in the past years, there is a need to optimize chemotherapeutic drugs dosing strategies to reduce toxicities, suboptimal responses, and the risk of relapse. Most cancer drugs have a narrow therapeutic index with substantial pharmacokinetics variability. Yet, current dosing approaches do not fully account for the complex pathophysiological characteristics of the patients. In this regard, the effect of sex on anticancer chemotherapeutic drugs disposition is still underexplored. In this article, we review sex differences in chemotherapeutic drug pharmacokinetics, we suggest a novel approach that integrates sex into the traditional a priori body-surface-area (BSA) dosing selection model and finally, we provide an overview of the potential benefits of a broader use of therapeutic drug monitoring (TDM) in oncology. Summary To date, anticancer chemotherapeutic drugs dosing is most often determined by BSA, a method widely used for of its ease-of-practice, despite criticism for not accounting for individual factors, notably sex. Anatomical, physiological, and biological differences between males and females can affect pharmacokinetics, including drug metabolism and clearance. At equivalent doses, females tend to display higher circulating exposure and more organ toxicities, which has been formally demonstrated at present for about 20% of chemotherapeutic drugs. An alternative could be the Sex-Adjusted-BSA (SA-BSA), incorporating a 10% increase in dosing for males and a 10% decrease for females, though this approach still lacks formal clinical validation. Another strategy to reduce treatment-related toxicity and potentially enhance clinical outcomes could be a more widespread use of therapeutic drug monitoring (TDM), for which a benefit has been demonstrated for 5-fluorouracil, busulfan, methotrexate or thiopurines.

Deciphering the Molecular Mechanism of Peracetic Acid Response in Listeria monocytogenes

Peracetic acid (PAA), a strong oxidizing agent, has been widely used as a disinfectant in food processing settings as it does not produce harmful chlorinated by-products. In the present study, the transcriptional response of Listeria monocytogenes to a sub-lethal concentration of PAA (2.5 ppm) was assessed using RNA-sequencing (RNA-seq). Our analysis revealed 12 differentially expressed protein-coding genes, of which nine were upregulated (ohrR, ohrA, rpsN, lmo0637, lmo1973, fur, lmo2492, zurM, and lmo1007), and three were down-regulated (argG, lmo0604 and lmo2156) in PAA-treated samples compared to the control samples. A non-coding small RNA gene (rli32) was also found to be down-regulated. In detail, the organic peroxide toxicity protection (OhrA-OhrR) system, the metal homeostasis genes fur and zurM, the SbrE-regulated lmo0636-lmo0637 operon and a carbohydrate phosphotransferase system (PTS) operon component were induced under exposure of L. monocytogenes to PAA. Hence, this study identified key elements involved in the primary response of L. monocytogenes to oxidative stress caused by PAA, including the expression of the peroxide detoxification system and fine-tuning the levels of redox-active metals in the cell. The investigation of the molecular mechanism of PAA response in L. monocytogenes is of utmost importance for the food industry, as residual PAA can lead to stress tolerance in pathogens.

Therapeutic Drug Monitoring of Antimicrobial Drugs in Children with Cancer: A New Tool for Personalized Medicine.

The risk of fungal, bacterial, and viral infections is higher in children with hematological and solid malignancies, particularly during periods of profound neutropenia. Although early administration of antimicrobial agents is common, optimizing pharmacological therapy in pediatric patients with cancer is challenging because of their variable pharmacokinetics compared with adults, including differences in body mass and augmented renal clearance, as well as chemotherapy-induced organ toxicity. Therapeutic drug monitoring, which involves measuring drug concentrations in serum or plasma at specific timepoints and adjusting doses accordingly, can be applied to various medications. While standardized targets for all antimicrobial agents in children are lacking, therapeutic drug monitoring appears to be beneficial in preventing serious toxicity and addressing treatment failure or non-compliance. This narrative review aims to analyze current perspectives on therapeutic drug monitoring for antimicrobial drugs in the special population of children with hematological or oncological diseases, including those undergoing hematopoietic cell transplantation. The review provides evidence on the clinical benefits of this method and explores potential future developments in this area.

Organ toxicities associated with diet-induced obesity in rats: Investigation of changes in activities selected enzymes.

Obesity stands out as one of the most significant health problems in the modern world. The prevalence of high-calorie diets (HCDs) globally exacerbates this condition. Throughout history, plants and plant-derived food products have been utilized for medicinal purposes, demonstrating their efficacy in the treatment and prevention of various diseases. Gundelia tournefortii (GT), a plant of interest, is known to possess beneficial properties. Hence, this study aimed to investigate the immunotoxic and neurotoxic effects of two different doses of GT plant extract on the liver, brain, and heart tissues of obese rats. For this purpose, Wistar male rats were divided into four groups: "CG," "HCDG," "HCDGUN1," and "HCDGUN2" At the conclusion of the study, adenosine deaminase (ADA) and myeloperoxidase (MPO) activities, as well as acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) biomarkers, were evaluated in the liver, heart, and brain tissues. The study results revealed a statistically significant increase in ADA and MPO activities in the HCDG group compared to the CG group, alongside a significant decrease in the HCDGUN groups compared to the HCDG group. Regarding AChE and BChE activities, a statistically significant decrease was observed in the HCDG group compared to the CG group, whereas an increase was noted in the HCDGUN groups relative to the HCDG group, with the latter approaching values similar to those of the control group. In conclusion, the intake of GT plant extract exhibited positive effects on the immunotoxic and neurotoxic effects induced by HCD in rats with an experimental obesity model, as evidenced by tissue biomarker evaluations.

Prediction of Organs Toxicity during CAR T-Cell Therapy By Using Cell-Free DNA Markers

Prediction of Organs Toxicity during CAR T-Cell Therapy By Using Cell-Free DNA Markers

Bridging organ transcriptomics for advancing multiple organ toxicity assessment with a generative AI approach

Translational research in toxicology has significantly benefited from transcriptomic profiling, particularly in drug safety. However, its application has predominantly focused on limited organs, notably the liver, due to resource constraints. This paper presents TransTox, an innovative AI model using a generative adversarial network (GAN) method to facilitate the bidirectional translation of transcriptomic profiles between the liver and kidney under drug treatment. TransTox demonstrates robust performance, validated across independent datasets and laboratories. First, the concordance between real experimental data and synthetic data generated by TransTox was demonstrated in characterizing toxicity mechanisms compared to real experimental settings. Second, TransTox proved valuable in gene expression predictive models, where synthetic data could be used to develop gene expression predictive models or serve as “digital twins” for diagnostic applications. The TransTox approach holds the potential for multi-organ toxicity assessment with AI and advancing the field of precision toxicology.

Antioxidant and Protective Effects of Oleaster Oil Against Silica Nanoparticle-Induced Oxidative Stress and Organ Toxicity in Rats

Nanoparticles have found widespread application in a variety of fields, despite growing worry about their possible hazardous effects on both the environment and human health. In recent years, research efforts have focused on plants and vegetable oils, which have been identified as abundant sources of many bioactive compounds. Many of these substances are known to participate in antioxidant processes. As a result, the current study was designed to investigate the antioxidant and protective properties of oleaster oil against cytotoxicity and oxidative stress induced by silica nanoparticles (SiNPs) in albino Wistar rats. Forty male rats were randomly assigned to four equally sized cohorts: a control group, SiNP-treated group (at a dose of 50 mg/kg), SiNP-treated group supplemented with oleaster oil (at a dose of 2 mL/kg), and those receiving only 2 mL/kg of oleaster oil. The findings demonstrated that SiNPs initiated an oxidative stress environment, as evidenced by higher lipid peroxidation levels and changes in antioxidant defense mechanisms. Antioxidant enzymes were significantly reduced, including glutathione levels between the control and SiNP-exposure treatments (36.01%, 36.59%, 60%), glutathione-S-transferase (29.74%, 29.90%, 13.49%), catalase (24.14%, 28.19%, 30.85%), and tissue superoxide dismutase (11.90%, 37.78%, 37.79%) in the liver, kidney, and heart, respectively. Furthermore, histological investigations revealed significant liver, kidney, and heart damage, as indicated by pathological alterations such as vascular dilatation and congestion, inflammatory cellular infiltration, and hepatocellular dysfunction. Encouragingly, the administration of oleaster oil significantly ameliorated a majority of these detrimental effects. These data suggest a potential protective effect of oleaster oil against the adverse histological effects induced by SiNP injection.

Transgenerational response of glucose metabolism in Caenorhabditis elegans exposed to 6-PPD quinone

In Caenorhabditis elegans, 6-PPD quinine (6-PPDQ) could cause several aspects of toxicity together with alteration in glucose metabolism. However, transgenerational alteration in glucose metabolism remains still unknown after 6-PPDQ exposure. In the current study, we further observed transgenerational increase in glucose content induced by 6-PPDQ (1–10 μg/L). After 1–10 μg/L 6-PPDQ exposure, although expressions of genes controlling gluconeogenesis were not changed in the offspring, expressions of hxk-1, hxk-3, pyk-1, and pyk-2 controlling glycolysis could be decreased in the offspring. Meanwhile, transgenerational decrease in expressions of daf-16 encoding FOXO transcriptional factor and aak-2 encoding AMPK was detected in the offspring of 6-PPDQ (1–10 μg/L) exposed nematodes. RNAi of daf-16 and aak-2 led to more severe transgenerational increase in glucose content and reduction in expressions of hxk-1 and hxk-3 induced by 6-PPDQ. Moreover, RNAi of daf-16, aak-2, hxk-1, hxk-3, pyk-1, and pyk-2 caused susceptibility to transgenerational 6-PPDQ toxicity on locomotion and reproduction. Additionally, 6-PPDQ induced activation of SOD-3 and HSP-6 reflecting anti-oxidation and mitochondrial UPR responses could be inhibited by RNAi of daf-16, aak-2, hxk-1, hxk-3, pyk-1, and pyk-2. Therefore, exposure to 6-PPDQ potentially resulted in transgenerational alteration in glucose metabolism, which provided the possible link to induction of transgenerational 6-PPDQ toxicity in organisms.

Leveraging Metabolomics and Ionomics to Illuminate Aluminum-Induced Toxicity in Mouse Organs

Aluminum, a widely prevalent environmental pollutant, has been established to exert toxic effects on multiple organs in the human body. To gain a comprehensive understanding of these toxic effects and the mechanisms involved, this study aimed to assess potential correlations between metabolites and ion data through metabolomic and ionomic analyses. We sought to explore the intricate impact of aluminum on various organs in mice. Gas chromatography-mass spectrometry (GC-MS) and inductively coupled plasma-mass spectrometry (ICP-MS) were employed to conduct metabolomic and ionomic analyses on the hippocampus, cortex, heart, liver, spleen, lung, kidney, bone, intestine, stomach, and serum of both control and aluminum-exposed mice. Besides, histological examinations and behavioral experiments were conducted. Multivariate analysis revealed 91 differential metabolites across various organs, primarily encompassing amino acids, fatty acids, and carbohydrates. The implicated abnormal metabolic pathways included amino acid metabolism, arachidonic acid metabolism, and glutathione metabolism. Additionally, alterations in the homeostasis of ions such as manganese, zinc, selenium, iron, copper, phosphorus, magnesium, and calcium were observed in various organs, potentially influencing the activity of critical enzymes. The changes in these potential biomarkers and ions suggest toxic mechanisms of aluminum exposure involving oxidative stress, inflammatory responses, cellular signal dysregulation, disruption of key enzyme activities, and impaired energy metabolism. This study provides a novel perspective on understanding the toxic mechanisms of aluminum exposure, potentially contributing to the prevention and treatment of aluminum toxicity.

Photodynamic-therapy and chemotherapy of TPBC-PEG nanoplatform encapsulated triptolide synergistically inhibit primary osteosarcoma growth and pulmonary metastasis by activating HIPPO signaling

Osteosarcoma is the most common bone malignancy in children and adolescents with a less than 30% overall survival rate for those with metastatic disease, particularly pulmonary metastases. Drug resistance hinders the effectiveness of current chemotherapies, making osteosarcoma a leading cause of mortality and an urgent requirement of new therapeutics in this population. Here, we developed a triptolide (TP)-loaded, pH-responsive and near-infrared light-activated nanoplatform (TP-TPBC-PEG) with photodynamic therapy (PDT) to target osteosarcoma cells both in vitro and in vivo. Our results demonstrated that PDT and chemotherapy of TP-TPBC-PEG synergistically reduced cell viability, colony proliferation, migration, and invasion in vitro, and inhibited osteosarcoma growth and pulmonary metastasis in vivo which the nano-micelles were intravenously injected to intratibia injection induced osteosarcoma mouse models, showing enhanced osteosarcoma cell killing by nanoparticle inflating in response to acidic endosomal pH and sensitized osteosarcoma cells to TP chemotherapy. Importantly, the nano-micelles did not exhibit organ toxicity in vivo. Dual-luciferase reporter gene and nuclear/ cytoplasm protein expression assays identified the involvement of HIPPO signaling pathway in mediating these effects. Overall, our study provides a promising therapeutic approach for treating primary osteosarcoma and preventing pulmonary metastases by activating the HIPPO signaling pathway.

Identifying in vitro toxicity testing approaches for (novel) proteins in the context of food and feed risk assessment

Abstract This report documents the outcomes of the EFSA procurement (OC/EFSA/NIF/2022/01) aimed at identifying in vitro toxicity testing approaches for (novel) proteins in the context of food and feed safety assessment. In the present report, we present an integrated testing strategy for the evaluation of toxicity of novel/toxic proteins. A text‐mining approach was used to create a literature database of toxic outcomes associated with toxic proteins retrieved from the UniProt KB database using the search term “Toxin activity”. It was shown that toxic proteins are produced by a relatively limited phylogenetic subset, including, among others, bacteria, insects, serpents, molluscs, and fungi. Toxicological effects of these proteins are generally conserved within phylogenetic groups. Analysis of toxic effects from these proteins was performed using GO term analysis as well as a text‐mining based approach. Relevant tests to address and quantify these toxicity effects were identified and evaluated for their applicability in an in vitro based toxicity testing strategy. A stepwise approach was developed. As a first step, an initial in silico prediction of toxicity is carried out (Step 1). This is followed by a battery of in vitro assays to address the primary mechanisms of toxicity associated with toxic proteins (Step 2). If concern arises in the Step 2 battery of tests, the use of relevant in vitro model systems to explore potential target organ toxicity are required (Step 3). Knowledge gaps have been identified and recommendations are provided in in vitro toxicity testing strategies, in particular for (novel) proteins. Some of these gaps involve the selection and integration of a standardized, relevant in vitro digestion step, reflective of passage through the digestive tract, within the testing strategy, as well as a thorough assessment of the suitability and applicability of in vitro tests and new approach methodologies for regulatory toxicity assessment of (novel) proteins. To accelerate the incorporation of NAMs in the assessment of protein safety, case studies and proof of concept projects are needed to demonstrate the utility and effectiveness of in vitro toxicity testing strategies in the safety assessment of (novel) proteins.

Folic-acid-targeted drug delivery system implementing Angelica gigas polysaccharide: A potential strategy for colorectal cancer treatment.

The study focuses on the development of folate-targeted conjugates utilizing Angelica gigas polysaccharide (F2) as a drug carrier for colorectal cancer therapy. We synthesized F2-C-5-FU conjugates by linking carboxymethyl-5-fluorouracil (C-5-FU) with folic acid (FA) through ester bonding. The drug release behavior of F2-C-5-FU-FA was pH-dependent, favoring release under alkaline conditions. After 96 h in phosphate buffer (pH 7.4), the conjugate exhibited a cumulative release of 54.7 %, which was higher compared to other pH environments. In vitro, F2-C-5-FU-FA showed enhanced cytotoxicity and increased cellular uptake in folate receptor-positive HCT-116 cells compared to A549 cells. The conjugate also induced G2/M cell cycle arrest and modulated the BAX/BCL-2 mRNA expression ratio through the MAPK and NF-κB signaling pathways. In vivo, F2-C-5-FU-FA increased tumor fluorescence intensity, prolonged drug circulation, and reduced organ toxicity to non-target organs. The treatment promoted cancer cell apoptosis by inhibiting the expression of apoptosis-related proteins. Overall, F2-C-5-FU-FA conjugates demonstrate potential as an effective drug delivery system for targeted colorectal cancer therapy.

Increasing the stability and efficiency of an electrochemical ammonium separation system via state-of-charge (SoC) control

Ammonium ions in wastewater can induce toxicity in aquatic organisms and accelerate eutrophication. Therefore, the efficient removal of ammonium ions is necessary. The electrochemical ion separation method, based on an electrode with selectivity for ammonium ions, is a promising recovery technique that can efficiently adsorb and desorb ammonium ions. In this system, the electrode is composed of copper hexacyanoferrate (CuHCF) and silver (Ag), and ammonium ions are captured by the CuHCF electrode. However, the stability of the CuHCF electrode is not sufficient for continuous ammonium ion removal. We aim to report an improvement in the stability of this system realized through the use of the state-of-charge (SoC) control method. The stability of the system can be enhanced by using SoC control at only 60 % of the maximum capacity. After 300 cycles, the discharge capacity for the 60 % SoC approach remained at 55.8 %, showing a 10 % improvement in stability compared to the 100 % SoC method (45.8 %). Furthermore, in concentrated solutions with a ratio similar to that of domestic wastewater, the 60 % SoC control strategy exhibited ammonium removal capacity and selectivity comparable to that with 100 % SoC control but with higher energy efficiency (77 % reduction in energy consumption). These results indicate that the state-of-charge (SoC) control method can enhance both the stability and the efficiency of the electrochemical ammonium separation system.

Older Adults with Ph Negative Acute Lymphoblastic Leukemia: A Monocentric Experience on 57 Patients Focusing on Treatment Intensity and Age-Related Prognosis.

Background: Treating with curative intent elderly patients affected by acute lymphoblastic leukemia (ALL) is an unmet clinical need. Comorbidities, lower tolerance to organ toxicities, and poor disease-related prognostic features make it difficult to cure these patients. Objectives: To analyze the outcome of ALL elderly patients aged over 55 years treated intensively or with the best supportive care (BSC) over the last 20 years.

Brief Overview on Pathology of Blood and Urine

Clinical pathology is recognized as an essential component of the preclinical safety evaluation of test articles (new chemical entities, exploratory novel medicines, and xenobiotics), particularly in short- and medium-term toxicity studies. Traditionally, this evaluation includes clinical chemistry, coagulation, hematology, and urinalysis assessments. The findings of these assessments include details on the general state of health of the animals as well as target organs and general metabolic, adaptive, or harmful processes linked to test material exposure. Consequently, in the preclinical safety assessment of a test article, clinical pathology evaluations aid in the establishment of toxicological dose-response correlations. These findings hold significance and relevance for dose selection in long-term research, as well as for risk assessment and management when applied to humans. Guidance on the fundamentals of clinical pathology testing and interpretation in the species utilized in toxicological investigations is the aim of this chapter. In order to increase testing capacity and enhance its ability to identify more sensitive, early signals of drug-induced target organ toxicity or pathophysiology, the application of clinical pathology testing in preclinical safety assessment as well as the areas of development for novel biomarker implementation within the laboratory are discussed. Lastly, the significance of interpreting clinical pathology and combining the results with data from other studies is emphasized when assessing overall safety or risk assessment

Nanomedicine in Cancer Treatment: Mechanisms, Applications, and Future Directions

Nanomedicine, an emerging field at the intersection of nanotechnology and medicine, holds significant promise for revolutionizing cancer treatment. By utilizing materials at the nanoscale, ranging from 1 to 100 nanometers, nanomedicine offers a versatile platform for targeting tumors, improving drug delivery, and minimizing side effects. This paper explores the design and preparation of nanoparticles, including common materials like liposomes, polymers, metals, and quantum dots, as well as their mechanisms of targeted delivery through both passive and active methods. Key applications of nanomedicine are discussed, particularly in chemotherapy, immunotherapy, and imaging. Clinical progress is highlighted through examples such as FDA-approved drugs like Onivyde for pancreatic cancer and experimental treatments like BIND-014 for metastatic prostate cancer. Despite rapid advancements, significant challenges remain, particularly in scaling up production and ensuring batch consistency. Safety concerns, such as nanoparticle toxicity and unintended accumulation in organs, must be addressed through rigorous testing and design improvements. Ethical considerations and regulatory hurdles also pose obstacles to the widespread clinical adoption of nanomedicine. Looking forward, multifunctionalization and personalized nanomedicine represent key areas of future growth, offering the potential for highly individualized treatments that combine therapeutic and diagnostic capabilities. Continued research and collaboration across scientific disciplines will be crucial in overcoming current limitations and unlocking the full potential of nanomedicine for cancer treatment.

Nanoparticles to target asthma.

Asthma is a heterogeneous chronic lung disease that affects nearly 340 million people globally. Airway hyperresponsiveness, remodeling (thickening and fibrosis), and mucus hypersecretion are some hallmarks of asthma. With several current treatments having serious side effects from long-term use and a proportion of patients with uncontrolled asthma, there is an urgent need for new therapies. With an increasing understanding of asthma pathophysiology, there is a recognized need to target therapies to specific cell types of the airway, which necessitates the identification of delivery systems that can overcome increased mucus and thickened airways. Nanoparticles (NPs) that are highly customizable (material, size, charge, and surface modification) are a potential solution for delivery systems of a wide variety of cargoes (nucleic acids, proteins, and/or small molecules), as well as sole therapeutics for asthma. However, there is a need to consider the safety of the NPs in terms of potential for inflammation, toxicity, nonspecific targets, and accumulation in organs. Ongoing clinical trials using NPs, some FDA-approved for therapeutics in other diseases, provide confidence regarding the potential safety and efficacy of NPs in asthma treatment. This review highlights the current state of the use of NPs in asthma, identifying opportunities for further improvements in NP design and utilization for targeting this chronic lung disease.

Copper-doped orange peel biochar activated peroxydisulfate for efficient degrading tetracycline: The critical role of C-OH and Cu

The usage of biomass waste has aroused great concern in water purification. In this study, copper-doped orange peel biochar (Cu-OPB) prepared by one-step carbonization was firstly used to activate peroxydisulfate (PDS) to eliminate tetracycline (TC). The optimized Cu-OPB showed great activation ability for PDS and could degrade 93.7% of TC at pH 9.07. The presence of H2PO4−, Cl−, and HCO3− did not affect the degradation, while HA and SO42− inhibited TC degradation. SO4•−, •OH and 1O2 were confirmed as the primary active oxygen species in the Cu-OPB/PDS system. Moreover, Cu and the C-OH functional groups on the surface of Cu-OPB played a critical role in the activation by accelerating the electronic migration between Cu-OPB and PDS in the catalytic system. 15 possible intermediate products were found and three feasible degradation pathways were proposed. The toxicity of aquatic organisms of TC was reduced. Furthermore, Cu-OPB could be used as an economically efficient and environmentally friendly catalyst for PDS activation to degrade organic pollutants.