Showing papers on "Toxicity published in 2021"

Sources, characteristics, toxicity, and control of ultrafine particles: An overview

Abstract: Air pollution by particulate matter (PM) is one of the main threats to human health, particularly in large cities where pollution levels are continually exceeded. According to their source of emission, geography, and local meteorology, the pollutant particles vary in size and composition. These particles are conditioned to the aerodynamic diameter and thus classified as coarse (2.5–10 μm), fine (0.1–2.5 μm), and ultrafine (

Radiation therapy-associated toxicity: Etiology, management, and prevention.

Abstract: Radiation therapy (RT) is a curative treatment for many malignancies and provides effective palliation in patients with tumor-related symptoms. However, the biophysical effects of RT are not specific to tumor cells and may produce toxicity due to exposure of surrounding organs and tissues. In this article, the authors review the clinical context, pathophysiology, risk factors, presentation, and management of RT side effects in each human organ system. Ionizing radiation works by producing DNA damage leading to tumor death, but effects on normal tissue may result in acute and/or late toxicity. The manifestation of toxicity depends on both cellular characteristics and affected organs' anatomy and physiology. There is usually a direct relationship between the radiation dose and volume to normal tissues and the risk of toxicity, which has led to guidelines and recommended dose limits for most tissues. Side effects are multifactorial, with contributions from baseline patient characteristics and other oncologic treatments. Technological advances in recent decades have decreased RT toxicity by dramatically improving the ability to deliver RT that maximizes tumor dose and minimizes organ dose. Thus the study of RT-associated toxicity is a complex, core component of radiation oncology training that continues to evolve alongside advances in cancer management. Because RT is used in up to one-half of all patients with cancer, an understanding of its acute and late effects in different organ systems is clinically pertinent to both oncologists and nononcologists.

Cadmium as a testicular toxicant: A Review.

Abstract: Cadmium (Cd) is a toxic heavy metal with no known biological functions in the human body. Due to a considerably long biological half-life and very low rate of excretion, accumulation of Cd in different body organs (eg, liver, kidney, and testes) over time is associated with perturbed functioning of these organs. Recent studies have shown the extreme sensitivity of the testes to Cd toxicity. In testes, Cd has been reported to induce oxidative stress, apoptosis of spermatogenic cells, reduction in androgen production and sperm functions. Moreover, Cd in combination with other environmental toxicants may be responsible for the declining fertility of males in both animals and humans. Pinpointing how Cd toxicity affects various testicular processes will be imperative for the development of preventative measures to promote fertility among males. Therefore, in the present review, we summarize the recent findings related to the Cd-induced oxidative toxicity, apoptotic toxicity, steroidogenic toxicity, and spermatotoxicity, along with their possible mechanisms in testicular tissue of different animal species. In addition, the utilization of various antioxidant compounds, medicinal plants and other compounds for the management of Cd toxicity in testes is discussed.

Acute Toxicity of a Tire Rubber-Derived Chemical, 6PPD Quinone, to Freshwater Fish and Crustacean Species

Abstract: N-(1,3-Dimethylbutyl)-N′-phenyl-p-phenylenediamine-quinone, also known as 6PPD quinone, was recently identified as a toxic chemical that causes acute mortality in coho salmon following exposure to urban runoff. Despite its potential occurrence in receiving waters worldwide, there is no information about the toxicity of 6PPD quinone to other aquatic species. In this study, to assess the aquatic toxicity of 6PPD quinone to freshwater fish and crustacean species, we performed standardized 48–96 h acute toxicity tests of 6PPD quinone with four species (Danio rerio, Oryzias latipes, Daphnia magna, and Hyalella azteca). In contrast to the high toxicity observed in coho salmon in a previous study (24 h LC50 of 0.79 μg/L), 6PPD quinone did not exhibit acute lethal toxicity to any species at its maximum water solubility. The absence of acute lethality of 6PPD quinone to tested species indicates that the urban runoff toxicity observed for the species can be attributed to other chemicals. The observed large discrepancy in toxicity (by a factor of ∼100) might be due to the specific toxicity of 6PPD quinone to coho salmon. Further research is needed to reveal the underlying mechanisms of the observed difference, which will be useful for both urban runoff management and aquatic toxicology.

Effects of chronic glyphosate exposure on antioxdative status, metabolism and immune response in tilapia (GIFT, Oreochromis niloticus).

Abstract: Glyphosate (Gly) is an active ingredient of herbicide, its underlying toxicity on fish is still unclear. The aim of this study was to evaluate chronic toxicity of Gly on tilapia via determining antioxidative status, metabolism, inflammation and immune response. The fish were exposed to different concentrations of Gly (0, 0.2, 0.8, 4 and 16 mg/L) for 80 days. The blood, liver, gills and spleen were collected to assay biochemical parameters and genes expression after 80 days of exposure. The results showed that treatments with higher Gly (4 and/16 mg/L) significantly increased the levels of TC, TG, AST, ALT, LDL-C and MDA, and apparently decreased the levels of SOD, GSH, CAT, HDL-C, HK, G3PDH, FBPase and G6PD in serum, liver and/or gills. The gene expression data showed that the treatments with Gly adversely affected Nrf2 pathway in liver, gills and spleen, as shown by significant changes of nrf2, keap1, ho-1, nqo1 and gsta mRNA levels. Meanwhile, inflammatory response was activated via enhancing the mRNA levels of nf-κb2, rel, rela tnf-α, and il-1β, and immunotoxicity was caused through downregulating the genes expression of c-lzm, hep, igm, hsp70 and c3 in liver, gills and/or spleen of tilapia after Gly exposure. Moreover, the mRNA levels of cyp1a and cyp3a were upregulated in 16 or 0.2 mg/kg Gly group in liver. Overall results suggested chronic Gly exposure reduced antioxidative ability, disturbed liver metabolism, promoted inflammation and suppressed immunity. Interestingly, the Nrf2 and NF-κB signaling pathways played key roles in Gly chronic toxicity.

Toxic Effects on Bioaccumulation, Hematological Parameters, Oxidative Stress, Immune Responses and Tissue Structure in Fish Exposed to Ammonia Nitrogen: A Review.

Abstract: Ammonia nitrogen is the major oxygen-consuming pollutant in aquatic environments. Exposure to ammonia nitrogen in the aquatic environment can lead to bioaccumulation in fish, and the ammonia nitrogen concentration is the main determinant of accumulation. In most aquatic environments, fish are at the top of the food chain and are most vulnerable to the toxic effects of high levels of ammonia nitrogen exposure. In fish exposed to toxicants, ammonia-induced toxicity is mainly caused by bioaccumulation in certain tissues. Ammonia nitrogen absorbed in the fish enters the circulatory system and affects hematological properties. Ammonia nitrogen also breaks balance in antioxidant capacity and causes oxidative damage. In addition, ammonia nitrogen affects the immune response and causes neurotoxicity because of the physical and chemical toxicity. Thence, the purpose of this review was to investigate various toxic effects of ammonia nitrogen, including oxidative stress, neurotoxicity and immune response.

Potential protective roles of curcumin against cadmium-induced toxicity and oxidative stress.

Abstract: Curcumin, used as a spice and traditional medicine in India, exerts beneficial effects against several diseases, owing to its antioxidant, analgesic, and anti-inflammatory properties. Evidence indicates that curcumin might protect against heavy metal-induced organ toxicity by targeting biological pathways involved in anti-oxidation, anti-inflammation, and anti-tumorigenesis. Curcumin has received considerable attention owing to its therapeutic properties, and the mechanisms underlying some of its actions have been recently investigated. Cadmium (Cd) is a heavy metal found in the environment and used extensively in industries. Chronic Cd exposure induces damage to bones, liver, kidneys, lungs, testes, and the immune and cardiovascular systems. Because of its long half-life, exposure to even low Cd levels might be harmful. Cd-induced toxicity involves the overproduction of reactive oxygen species (ROS), resulting in oxidative stress and damage to essential biomolecules. Dietary antioxidants, such as chelating agents, display the potential to reduce Cd accumulation and metal-induced toxicity. Curcumin scavenges ROS and inhibits oxidative damage, thus resulting in many therapeutic properties. This review aims to address the effectiveness of curcumin against Cd-induced organ toxicity and presents evidence supporting the use of curcumin as a protective antioxidant.

The Toxicity, Pathophysiology, and Treatment of Acute Hydrazine Propellant Exposure: A Systematic Review

Abstract: Introduction Hydrazines are highly toxic inorganic liquids that are used as propellants in military and aviation industries, such as the U.S. Air Force F-16 Emergency Power Unit and SpaceX SuperDraco Rockets. The most commonly used derivatives include hydrazine, monomethylhydrazine, and 1,1-dimethylhydrazine (unsymmetrical dimethylhydrazine). Industrial workers in close contact with hydrazines during routine maintenance tasks can be exposed to levels well above the National Institute for Occupational Safety and Health relative exposure limits. Materials and methods A systematic review was performed using PubMed, Web of Science, Google Scholar, National Aeronautics and Space Administration Technical Server, and Defense Technical Information Center, and data related to hydrazine exposures were searched from inception to April 2020. Publications or reports addressing hydrazine toxicity, pathophysiology, and treatment of hydrazine fuel exposure were selected. Results Acute toxic exposures to hydrazine and its derivatives are rare. There are few case reports of acute toxic exposure in humans, and data are largely based on animal studies. The initial search identified 741 articles, manuscripts, and government reports. After screening for eligibility, 51 were included in this review. Eight articles reported acute exposures to hydrazine propellant in humans, and an additional 14 articles reported relevant animal data. Conclusions Exposure to small amounts of hydrazine and its derivatives can cause significant soft tissue injury, pulmonary injury, seizures, coma, and death. Neurologic presentations can vary based on exposure compound and dose. Decontamination is critical as treatment is mainly supportive. High-dose intravenous pyridoxine has been suggested as treatment for hydrazine-related neurologic toxicity, but this recommendation is based on limited human data. Despite recent research efforts to generate less toxic alternatives to hydrazine fuel, it will likely continue to have a role in military and aviation industries. Aerospace and military physicians should be aware of the toxicity associated with hydrazine exposure and be prepared to treat hydrazine toxicity in at-risk populations.

Source, bioaccumulation, degradability and toxicity of triclosan in aquatic environments: A review

Abstract: Triclosan (TCS), a lipophilic broad-spectrum biocide is widely used in personal care, acrylic, veterinary, medical and household products. It has been observed to be present in aquatic environments, animal and plant tissues around the world, and even in human blood, urine and breast milk. Under natural conditions, TCS degrades photolytically as well as through microbial action into more persistent and toxic byproducts like dioxins. Moreover, accumulation in deep water bodies or soil strata where light is not adequately available makes its degradation even more prolonged. Present review has been undertaken with an objective to highlight the concerns surrounding TCS exposure to aquatic organisms, the infiltration routes into the food chain, its persistence and accumulation, teratogenic, biochemical and cytogenic effects on a wide range of aquatic species. The widespread use of products containing TCS and potential toxicity at lethal concentrations makes it a compound of utmost concern worldwide and hence its use under permissible levels, proper disposal needs to be regulated.

Involvement of cytochrome P450 enzymes in inflammation and cancer: a review

Abstract: Cytochrome P450 (CYP) enzymes are responsible for the biotransformation of drugs, xenobiotics, and endogenous substances. This enzymatic activity can be modulated by intrinsic and extrinsic factors, modifying the organism's response to medications. Among the factors that are responsible for enzyme inhibition or induction is the release of proinflammatory cytokines, such as interleukin-1 (IL-1), IL-6, tumor necrosis factor α (TNF-α), and interferon-γ (IFN-γ), from macrophages, lymphocytes, and neutrophils. These cells are also present in the tumor microenvironment, participating in the development of cancer, a disease that is characterized by cellular mutations that favor cell survival and proliferation. Mutations also occur in CYP enzymes, resulting in enzymatic polymorphisms and modulation of their activity. Therefore, the inhibition or induction of CYP enzymes by proinflammatory cytokines in the tumor microenvironment can promote carcinogenesis and affect chemotherapy, resulting in adverse effects, toxicity, or therapeutic failure. This review discusses the relevance of CYPs in hepatocarcinoma, breast cancer, lung cancer, and chemotherapy by reviewing in vitro, in vivo, and clinical studies. We also discuss the importance of elucidating the relationships between inflammation, CYPs, and cancer to predict drug interactions and therapeutic efficacy.

Resveratrol-loaded nanomedicines for cancer applications.

Abstract: Background Resveratrol (3, 5, 4' -trihydroxystilbene), a natural polyphenol and phytoalexin, has drawn considerable attention in the past decade due to its wide variety of therapeutic activities such as anticancer, anti-inflammatory, and antioxidant properties. However, its poor water solubility, low chemical stability, and short biological half-life limit its clinical utility. Recent findings Nanoparticles overcome the limitations associated with conventional chemotherapeutic drugs, such as limited availability of drugs to the tumor tissues, high systemic exposures, and consequent toxicity to healthy tissues. This review focuses on the physicochemical properties of resveratrol, the therapeutic potential of resveratrol nano-formulations, and the anticancer activity of resveratrol encapsulated nanoparticles on various malignancies such as skin, breast, prostate, colon, liver, ovarian, and lung cancers (focusing on both in vitro and in vivo studies). Conclusions Nanotechnology approaches have been extensively utilized to achieve higher solubility, improved oral bioavailability, enhanced stability, and controlled release of resveratrol. The resveratrol nanoparticles have markedly enhanced its anticancer activity both in vitro and in vivo, thus considering it as a potential strategy to fight various cancers.

Hesperidin protects against the chlorpyrifos-induced chronic hepato-renal toxicity in rats associated with oxidative stress, inflammation, apoptosis, autophagy, and up-regulation of PARP-1/VEGF.

Abstract: In this study, we investigated the effects of hesperidin (HSP) on oxidants/antioxidants status, inflammation, apoptotic, and autophagic activity in hepato-renal toxicity induced by chronic chlorpyrifos (CPF) exposure in rats. We used a total of 35 male albino rats in five groups of seven: control, HSP 100, CPF, CPF + HSP50, and CPF + HSP100. After rats were sacrificed, blood, liver, and kidney samples were collected. Serum levels of aspartate aminotransferases (ALT and AST), alkaline phosphatase (ALP), creatinine, and urea were tested. Then, contents of the superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), glutathione peroxidase (GPx), and glutathione (GSH) were measured to detect the level of oxidative stress in rat liver and renal tissues. We measured inflammatory and autophagy markers of chlorpyrifos induced oxidative stress in the liver and kidney tissues including TNF-α, iNOS, IL-1 β, COX-2, NF-κB, MAPK14, and Beclin-1 using ELISA. Histopathological findings were also examined followed by immunohistochemical determination of 8-OHdG expression. Real-time PCR (RT-PCR) was used to examine Cas-3, Bax, Bcl-2, PARP-1, and VEGF, which are associated with apoptosis, autophagy, DNA, and endothelial damage, respectively. In addition, PARP-1 activity was supported by western blot and immunofluorescence, VEGF activity was supported by western blot methods. Treatment with HSP reduced the effect of CPF on ALT, AST, ALP, and total proteins, and increased its effect on tissue antioxidants. PARP/VEGF, apoptotic, pro-apoptotic, anti-apoptotic, and autophagic gene expressions were regulated, and Caspase-3 and Bax expressions were decreased; Bcl-2 expression increased in both the liver and kidney samples, and positivity of 8-OHdG and PARP-1 were reduced in the CPF plus HSP-treated group. Overall, the study demonstrates that HSP may reduce the effects of hepato-renal toxicity caused by CPF by regulating oxidative stress, inflammation, apoptosis, autophagy, and PARP/VEGF genes at biochemical, cellular, and molecular levels.