Oxidative Organ Damage Research Articles

Toxicological screening of zinc oxide nanoparticles in mongrel dogs after seven days of repeated subcutaneous injections

Zinc oxide nanoparticles (ZnO NPs) have recently been applied in various veterinary and medical fields, however, the toxicological evaluations of these NPs in dogs are lacking. Therefore, the current study is designed to assess the impact of exposure to daily subcutaneous (SC) injections of ZnO NPs at different concentrations on various organs of mongrel dogs. Nine dogs were randomly divided into three groups (n = 3 for each) as follows: group (1) served as the control group, whereas groups (2&3) received SC injections of 50 and 100 ppm ZnO NPs (8 and 16 μg/kg bwt), respectively, once/day for 7 days. Our results revealed that ZnO NPs disrupted the oxidant/antioxidant balance in the lungs, liver, and kidneys of dogs in a dose-dependent manner. ZnO NPs induced dose-dependent radiological, ultrasonographical, and histopathological alterations in various organs especially lungs, spleen, liver, and kidneys along with disturbance in both liver and kidney biomarkers levels. Most organs of both ZnO NPs receiving groups displayed strong caspase-3 protein expression. Additionally, it upregulates the transcriptase levels of TNF-α and VEGF, as well as downregulates the antiapoptotic gene IL-10 in lung, kidney, and liver tissue homogenates. It was concluded that the daily SC injections of dogs with ZnO NPs at concentrations of 50 and 100 ppm caused extensive oxidative stress damage in various organs which provoked serious pathological processes such as apoptosis and inflammation.

Pharmacological Activities of Plant-Derived Fraxin with Molecular Mechanisms: A Comprehensive Review.

Fruits and vegetables serve not only as sources of nutrition but also as medicinal agents for the treatment of diverse diseases and maladies. These dietary components are significant resources of phytochemicals that demonstrate therapeutic properties against many illnesses. Fraxin is a naturally occurring coumarin glycoside mainly present in various species of Fraxinus genera, having a multitude of therapeutic uses against various diseases and disorders. This study focuses to investigate the pharmacological activities, botanical sources, and biopharmaceutical profile of the phytochemical fraxin based on different preclinical and non-clinical studies to show the scientific evidence and to evaluate the underlying molecular mechanisms of the therapeutic effects against various ailments. For this, data was searched and collected (as of February 15, 2024) in a variety of credible electronic databases, including PubMed/Medline, Scopus, Springer Link, ScienceDirect, Wiley Online, Web of Science, and Google Scholar. The findings demonstrated favorable outcomes in relation to a range of diseases or medical conditions, including inflammation, neurodegenerative disorders such as cerebral ischemia-reperfusion (I/R) and depression, viral infection, as well as diabetic nephropathy. The phytochemical also showed protective effects such as osteoprotective, renoprotective, pulmoprotective, hepatoprotective, and gastroprotective effects due to its antioxidant capacity. Fraxin has a great capability to diminish oxidative stress-related damage in different organs by stimulating the antioxidant enzymes, downregulating nuclear factor kappa B and NLRP3, and triggering the Nrf2/ARE signaling pathways. Fraxin exhibited poor oral bioavailability because of reduced absorption and a wide distribution into tissues of different organs. However, extensive research is required to decipher the biopharmaceutical profiles, and clinical studies are necessary to establish the efficacy of the natural compound as a reliable therapeutic agent.

Biogenic crocetin-crosslinked chitosan nanoparticles with high stability and drug loading for efficient radioprotection

The risk of radiation exposure increases with the development of nuclear energy and technology, and radiation protection receives more and more attention from public health and safety. However, the numerous adverse effects and low drug utilization limit the practical applications of radioprotective agents. In this study, we developed a biogenic crocetin-crosslinked chitosan nanoparticle with high stability and drug loading for efficient radioprotection. In detail, the nanoparticles were prepared using the natural antioxidant crocetin as a cross-linking reagent in amidation reactions of chitosan and mPEG-COOH. The nanoparticles exhibit a quick scavenging ability for common reactive oxygen species and reactive nitrogen in vitro. Meanwhile, cellular experiments demonstrate the good biocompatibility of the nanoparticles and the alleviation of radiation damage by scavenging reactive oxygen species, reducing apoptosis, and inhibiting DNA damage, etc. Importantly, the nanoparticles are effective in mitigating oxidative damage in major organs and maintaining peripheral blood cell content. In addition, they perform better radioprotective properties than free drug due to the significant extension of the blood half-life of crocetin in vivo from 10 min to 5 h. This work proposes a drug-crosslinking strategy for the design of a highly efficient radioprotective agent, which exhibits a promising prospect in the fields of nuclear emergency and public health.

Cafeteria diet can cause systemic inflammation and oxidative damage in the various tissues

BACKGROUND: Cafeteria diet (CAF) is a succesful tool for establishing animal obesity model. This study purposed to show immunoexpression and oxidant-antioxidant status in the various organ tissues of Wistar rats fed CAF. METHODS: Two groups (six rats per group) of Wistar albino rats were fed CAF and standard chow (control) diets for eight weeks. After experimental procedure, the animals were sacrificed. Intestine, stomach, liver, kidney, spleen, heart, lung, and pancreas tissues were sent to Pathology Department and inducible nitric oxide synthase (iNOS), nuclear factor- κB (NF-κB) and cannabinoid receptor-1 (CB-1) immunoexpressions were assessed. Also, plasma liver function tests and lipid levels were measured total oxidant capacity (TOC) and total antioxidant capacity (TAC) were evaluated in both plasma and liver tissue. RESULTS: The immunoexpressions of NF-κB, iNOS and CB-1 were higher in the experiment group for all tissues. TOC was significantly higher in the experiment group, for both plasma and liver tissue (p < 0.001 and p = 0.02). TAC was higher in the experiment group’s plasma measurement (p = 0.02), while there was no difference in the liver tissue between experiment and control groups (p = 0.11). CONCLUSION: CAF-induced obesity may be related to increased immunoexpression and oxidative damage in the various organs. Systemic problems should be considered and these phenomenon should be studied more comprehensively.

Preparation and Hemocompatibility of Novel Antioxidant-Modified Polyethersulfone Membranes as Red Blood Cell Thrombosis Inhibitors.

The contact between the dialysis membrane and blood can induce oxidative stress and thrombosis, causing oxidative organ damage and impaired toxin clearance. To date, the selection of anticoagulants has focused on mechanisms inhibiting white, but not red (erythrocytes) thrombus formation. In the present study, polyethersulfone (PES) membranes are modified with the antioxidant drug tiopronin; the physicochemical properties and dialysis performance of the Tio-PES membranes are evaluated. The effects on erythrocyte thrombosis are evaluated in terms of erythrocyte morphology, prothrombotic properties (adhesion, aggregation, viscosity, sedimentation, and hemolysis), and fibrinogen (FIB)-erythrocyte interactions. The regular anticoagulant and antiplatelet properties are also assessed. Superoxide dismutase, malondialdehyde, plasma protein, and complement C3a are further determined. Finally, the biosafety of the Tio-PES membranes is evaluated both in vitro and in vivo. The Tio-PES membranes exhibit excellent physicochemical properties and improved dialysis performance. It is found that the Tio-PES membranes stabilize erythrocyte morphology, reduce erythrocyte prothrombotic properties, decrease FIB adsorption, and prevent red thrombus formation. In addition, the Tio-PES membranes exhibit excellent antioxidant properties and show biosafety in primary toxicity studies. Thus, Tio-PES membranes hold promise as novel, safe, and effective dialysis materials for potential clinical application.

Antiplasmodial Activity of β-Ionone and the Effect of the Compound on Amelioration of Anaemia and Oxidative Organ Damage in Mice Infected with Plasmodium berghei.

Owing to evolution of parasite strains that are resistant to existing antimalarial drugs, research for novel antimalarial medicines is progressing on numerous fronts. Herein, we evaluated the in vivo anti-Plasmodium berghei activity of β-ionone including its ameliorative potential towards P. berghei-associated anaemia and oxidative organ damage. Mice were infected with chloroquine-sensitive strain of P. berghei and then treated with β-ionone at doses of 10 and 20mg/kg body weight (BW) for seven days. The parasitemia, packed cell volume and redox sensitive biomarkers in the liver, brain and spleen were estimated. Our result showed that β-ionone, in a dose-dependent fashion, significantly (p < 0.05) repressed the multiplication of P. berghei. More so, the compound, at doses of 10 and 20mg/kg BW, significantly (p < 0.05) mitigated anaemia and organ damage induced by P. berghei. Overall, the findings demonstrated that β-ionone has antiplasmodial actions and plays a mitigative role against P. berghei-induced anaemia and oxidative organ damage.

Effect of Boric Acid on Oxidative Damage in Immunocompetent Organs under Conditions of Potassium Bichromate and Gamma Radiation Exposure

The immune system supports antigenic homeostasis in the body and regulates the processes of proliferation and differentiation of cellular components in hemo- and immunopoiesis. Chromium compounds and ionizing radiation lead to the formation of highly reactive free radicals. Sublethal dose of gamma-irradiation is characterized by a 56% decrease in thymus cellularity and a 22% decrease in lymph nodes against the background of a 44% increase in the number of lymphoid cells in the spleen. Under the combined effect of hexavalent chromium and gamma-radiation, a decrease in the number of lymphoid cells is observed. In thymus the cellularity decreases by 70%, in spleen - by 40%, in lymph nodes - by 42% in comparison with control data. Under the influence of boric acid the number of lymphoid cells in thymus significantly increases by 47%, in lymph nodes - by 14% (p&lt;0.05) compared to the data of irradiated animals. Boric acid administration weakens the development of oxidative stress, lipid peroxidation decreases, and the activity of antioxidant defense enzymes in immunocompetent cells is increased.

Aflatoxin B1-induced early developmental hepatotoxicity in larvae zebrafish

Aflatoxin B1 (AFB1) is a ubiquitous mycotoxin that causes oxidative damage in various organs. At present, the research studies on AFB1 are primarily focused on its effects on the terrestrial environment and animals. However, its toxicity mechanism in aquatic environments and aquatic animals has not been largely explored. Thus, in this study, zebrafish was used as a model to study the toxicity mechanism of AFB1 on the liver of developing larvae. The results showed that AFB1 exposure inhibited liver development and promoted fat accumulation in the liver. Transcriptome sequencing analysis showed that AFB1 affected liver redox metabolism and oxidoreductase activity. KEGG analysis showed that AFB1 inhibited the expression of gsto1, gpx4a, mgst3a, and idh1 in the glutathione metabolizing enzyme gene pathway, resulting in hepatic oxidative stress. At the same time, AFB1 also inhibited the expression of acox1, acsl1b, pparα, fabp2, and cpt1 genes in peroxidase and PPAR metabolic pathways, inducing hepatic steatosis and lipid droplet accumulation. Antioxidant N-Acetyl-l-cysteine (NAC) preconditioning up-regulated gsto1, gpx4a and idh1 genes, and improved the AFB1-induced lipid droplet accumulation in the liver. In summary, AFB1 induced hepatic oxidative stress and steatosis, resulting in abnormal liver fat metabolism and accumulation of cellular lipid droplets. NAC could be used as a potential preventative drug to improve AFB1-induced fat accumulation.

Therapeutic activity of eugenol towards mitigation of anaemia and oxidative organ damage caused by Plasmodium berghei

The parasite responsible for causing malaria infection, Plasmodium, is known to exhibit resistance to a number of already available treatments. This has prompted the continue search for new antimalarial drugs ranging from medicinal plant parts to synthetic compounds. In lieu of this, the mitigative action of the bioactive compound, eugenol towards P. berghei-induced anaemia and oxidative organ damage was investigated following a demonstration of in vitro and in vivo antiplasmodial effects. Mice were infected with chloroquine-sensitive strain of P. berghei and thereafter treated with eugenol at doses of 10 and 20 mg/kg body weight (BW) for seven days. The packed cell volume and redox sensitive biomarkers in the liver, brain and spleen were measured. Our result demonstrated that eugenol significantly (p < 0.05) ameliorated the P. berghei-associated anaemia at a dose of 10 mg/kg BW. In addition, the compound, at a dose of 10 mg/kg BW, significantly (p < 0.05) alleviated the P. berghei-induced organ damage. This evidently confirmed that eugenol plays an ameliorative role towards P. berghei-related pathological alterations. Hence, the study opens up a new therapeutic use of eugenol against plasmodium parasite.

Engineering Therapeutics to Detoxify Hemoglobin, Heme, and Iron.

Hemolysis (i.e., red blood cell lysis) can increase circulatory levels of cell-free hemoglobin (Hb) and its degradation by-products, namely heme (h) and iron (Fe). Under homeostasis, minor increases in these three hemolytic by-products (Hb/h/Fe) are rapidly scavenged and cleared by natural plasma proteins. Under certain pathophysiological conditions, scavenging systems become overwhelmed, leading to the accumulation of Hb/h/Fe in the circulation. Unfortunately, these species cause various side effects such as vasoconstriction, hypertension, and oxidative organ damage. Therefore, various therapeutics strategies are in development, ranging from supplementation with depleted plasma scavenger proteins to engineered biomimetic protein constructs capable of scavenging multiple hemolytic species. In this review, we briefly describe hemolysis and the characteristics of the major plasma-derived protein scavengers of Hb/h/Fe. Finally, we present novel engineering approaches designed to address the toxicity of these hemolytic by-products.

Effects of Salacia Oblonga on aluminium induced changes on membrane ATPases of various organs in Wistar albino rats

Background: Aluminium, one of the abundant elements present in nature enters human body through diet, food packaging material and medication. Aluminium can induce toxicity by causing oxidative damage and by altering the function of membrane bound ATPases, Salacia oblonga, a woody climbing plant with vast geographical distribution in India possess various biological functions. Previous studies have shown a protective effect of S. oblonga on Al induced visceral toxicity. Our aim is to evaluate the effect of S. oblonga extract on aluminium induced oxidative organ damage and haematological changes Methods: The experimental animals, Wistar albino rats, were divided into four groups of 6 per group. The four groups are divided into distilled water, Aluminium chloride, Salacia oblonga extract and aluminium and Salacia oblonga. On 37th day animals were sacrificed and organs and blood were collected for assessment of ATPase activity, protein levels and haematological parameters. Results: Salacia oblonga increased the ATPase activity in the brain, heart and lungs, improved the protein levels and haematological parameters which were deteriorated by Al toxicity. Though statistically insignificant S. oblonga improved the ATPase enzymes and haematological parameters. Conclusions: Our study demonstrated that Aluminium causes membrane damage in various organs by altering the membrane ATPases level as a result of oxidative stress and altered the haematological parameters. We demonstrated that S. oblonga ameliorates Al induced membrane toxicity and also confers hemoprotective effect.

AMF species do matter: Rhizophagus irregularis and Funneliformis mosseae affect healthy and PVY-infected Solanum tuberosum L. in a different way.

Arbuscular mycorrhizal fungi (AMF) were documented to positively influence plant growth and yield, which is extremely important for the production of many crops including potato. However, the nature of the interaction between arbuscular mycorrhiza and plant virus that share the same host is not well characterized. In this study, we examined the effect of different AMF, Rhizophagus irregularis and Funneliformis mosseae, on healthy and potato virus Y (PVY)-infected Solanum tuberosum L. The analyses conducted included the measurement of potato growth parameters, oxidative stress indicators, and photosynthetic capacity. Additionally, we evaluated both the development of AMF in plant roots and the virus level in mycorrhizal plants. We found that two AMF species colonized plant roots to varying degrees (ca. 38% for R. irregularis vs. 20% for F. mosseae). Rhizophagus irregularis had a more positive effect on potato growth parameters, causing a significant increase in the total fresh and dry weight of tubers, along with virus-challenged plants. Furthermore, this species lowered hydrogen peroxide levels in PVY-infected leaves and positively modulated the levels of nonenzymatic antioxidants, i.e., ascorbate and glutathione in leaves and roots. Finally, both fungal species contributed to reduced lipid peroxidation and alleviation of virus-induced oxidative damage in plant organs. We also confirmed an indirect interaction between AMF and PVY inhabiting the same host. The two AMF species seemed to have different abilities to colonize the roots of virus-infected hosts, as R. irregularis showed a stronger drop in mycorrhizal development in the presence of PVY. At the same time, arbuscular mycorrhiza exerted an effect on virus multiplication, causing increased PVY accumulation in plant leaves and a decreased concentration of virus in roots. In conclusion, the effect of AMF-plant interactions may differ depending on the genotypes of both symbiotic partners. Additionally, indirect AMF-PVY interactions occur in host plants, diminishing the establishment of arbuscular mycorrhiza while changing the distribution of viral particles in plants.

Apohemoglobin-haptoglobin complex alleviates iron toxicity in mice with β-thalassemia via scavenging of cell-free hemoglobin and heme

β-thalassemia is a genetic hemoglobin (Hb) disorder that affects millions of people world-wide. It is characterized by ineffective erythropoiesis and anemia. The resultant chronic anemia can require life-long blood transfusion regimens, leading to secondary hemochromatosis. Moreover, the abnormal red blood cells (RBCs) from β-thalassemia patients are prone to hemolytic events that release cell-free Hb and heme causing a series of events that result in oxidative organ and tissue damage. In this study, β-thalassemic mice were treated with a protein scavenger for six weeks, apohemoglobin-haptoglobin (apoHb-Hp), this protein scavenges cell free Hb and heme. We hypothesize that scavenging cell-free Hb and heme will lead to a positive therapeutic event. After the apoHb-hp treatment it was observed to reduce the weight of the liver and spleen and show an improvement in liver function by a drop in ALT, AST, and ALP markers. ApoHb-hp treatment also hints at an improved RBC half-life as the number of reticulocytes decreased, the mean corpuscular volume (MCV) increased, mean corpuscular hemoglobin increase and the RBC distribution width decreased. Furthermore, apoHb-Hp treatment reduced circulating serum iron concentration and transferrin saturation concentration. Based on these outcomes, introducing a scavenger protein can benefit β-thalassemic mice. This study demonstrated that apoHb-Hp treatment may be a viable strategy to mitigate toxicities associated with cell free Hb and heme, a driver of β-thalassemic issues.

Bisphenol A induced oxidative damage in the rat reproductive organs: A possible cause for decline in steroidogenesis

Bisphenol A induced oxidative damage in the rat reproductive organs: A possible cause for decline in steroidogenesis

High Doses of Anacardium Occidentale Nut Shell Extract Induce Oxidative Damage in Cardiac and Renal Organs of Wistar Rats

Anacardium occidentale (Cashew) is a plant reported to show several biological activities. The aim of this study is to examine the effects of methanol extract of Anacardium occidentale nut shell on the antioxidant status and histological features in cardiac and renal tissues of rats. Shells were obtained from the nut, air-dried, pulverized, and subjected to Soxhlet extraction to obtain Anacardium occidentale nut shell extract (AONSE). Forty-five male Wistar rats were divided into nine groups (5 rats each), and given oral gavage of corn oil (Control), and 50, 100, 150, 200, 250, 300, 350 and 400 mg/kg of AONSE, every other day for twenty-eight days. After sacrifice, heart and kidney were removed and divided into two portions each; one portion was homogenized for biochemical assays, while the other was fixed in formalin for histopathology. Superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST) and Malondialdehyde (MDA) levels in the two organs were spectrophotometrically assayed. Histopathology of the organs was also done. The SOD and catalase were reduced in heart at high doses of AONSE relative to control. The AONSE has no significant effects on GPx, GST and MDA in the two organs, comparable to control. Photomicrographs of heart show, myocardial distortions and fibrosis, while glomerular fluid accumulation and hemorrhagic fibrosis were observed in kidney, at high doses, as against control and low doses of AONSE. This study shows that high doses of Anacardium occidentale nut shell extract could induce cytological derangements in heart and kidney of rats, possibly via oxidative mechanism.

High Doses of Anacardium Occidentale Nut Shell Extract Induce Oxidative Damage in Cardiac and Renal Organs of Wistar Rats

High Doses of Anacardium Occidentale Nut Shell Extract Induce Oxidative Damage in Cardiac and Renal Organs of Wistar Rats

The immunohistochemical investigation of chymase-, tryptase- and ghrelin-positive cells on the lung of rat after an application of Sambucus nigra

Sambucus nigra (S.nigra) is used in the treatment of many diseases and disorders thanks to its antioxidant, anticarcinogenic, immunostimulating, antiallergic, antiviral, and antibacterial properties. Ghrelin has anti-inflammatory effect on oxidative damage in various organs and cell types. The aim of this study was to immunohistochemically examine the chymase, tryptase, and ghrelin in rat lung after S. nigra administration. A total of 16 male rats were used in the study. The rats were assigned to two groups, control and S. nigra. 1st control group (n=8): No application was made. 2nd S. nigra group (n=8): S. nigra extract was administered at 15 mg/kg by oral gavage for 14 days. Tryptase, chymase, and ghrelin-positive cells were found in the lung tissue in a spindle-shaped, round, or oval shape. When the groups were evaluated within themselves, a significant increase in the number of tryptase, chymase, and ghrelin positive cells was observed in the S. nigra treated group. This study showed that S. nigra, which has an immunomodulatory and antioxidant effect, increases the expression of chymase-, tryptase- and ghrelin-positive cells in the lungs. Additionally, based on our findings, it can be said that mast cells can produce, store and release ghrelin.

Oxidative stress in multiple organs after sepsis in elderly rats.

Aging is a dynamic process, in which morphological and physiological changes occur at all levels, making the body more vulnerable to acute events. Elderly people are at greater risk of sepsis developing than younger people. Sepsis is a set of serious manifestations throughout the body produced by an infection, leading to events that compromise cell homeostasis as oxidative stress and is associated with organ dysfunction. The aim of this study was to evaluate multi-organ oxidative stress in old rats in an animal model of polymicrobial sepsis. Adult (60d) and old (210d) male Wistar rats were submitted to sepsis by cecal ligation and perforation (CLP) and control group (sham) only by laparotomy. The experimental groups were divided into sham 60d, sham 210d, CLP 60d and CLP 210d. Twenty-four hours after CLP, myeloperoxidase (MPO) activity, oxidative damage to lipids and proteins, superoxide dismutase (SOD) and catalase (CAT) activities were evaluated in the lung, kidney, liver, heart, spleen, quadriceps and diaphragm. Aging potentiated the increase in MPO activity in the after sepsis in the lung, liver and spleen. Lipid oxidative damage occurred in all structures analyzed in the CLP groups, while only in the lung, liver and diaphragm the lipid peroxidation was higher in the CLP 210d group compared to 60d. Regarding protein damage, this potentiation happened only in the lung. The SOD activity in the lung, kidney, spleen and diaphragm there was a significant decrease in the CLP 210d group compared to the sham 60d group while in the CAT only in the lung and kidney. The findings in this study indicate that increasing age potentiated oxidative damage in different organs after sepsis by intensifying the presence of neutrophils, which possibly increased the damage to lipids and proteins with reduced activity of SOD and CAT.

The Significance of Nitrosative Pressure in Underlying Pathophysiology and The Pharmacologic Therapy of Non-Communicable Disease with Fessional and Antioxidant Potential

Chronic stress (OS) can degrade a range of substances and cellular structures, impairing organ and system performance. Endogenous and external pathways contribute to the accumulation of OS in the body. There is mounting evidence that OS has a role in the physiopathology of various chronic disorders that require continuous pharmaceutical treatment. Prolonged therapy may affect systemic OS. We explore the role of OS in the pathophysiology of several chronic diseases, the pro- or antioxidant effects of their pharmaceutical therapies, and potential adjuvant antioxidant alternatives in this review. High blood pressure, arteriosclerosis, and diabetes mellitus raise the risk of developing cardiovascular disease. Antihypertensive, lipid-lowering, and hypoglycemic medications contribute to risk reduction while also providing an antioxidant benefit. In autoimmune systemic inflammatory illnesses such as rheumatoid arthritis, methotrexate treatment has a dual effect of boosting OS synthesis and causing mitochondrial malfunction. However, it may also contribute indirectly to reducing systemic OS caused by inflammation. Medications used to treat neurodegenerative illnesses have been shown to inhibit systems involved in producing and balancing reactive oxygen species (ROS). On the other hand, immunosuppressive treatments for cancer or human immunodeficiency virus infection enhance ROS generation, resulting in severe oxidative damage in several organs and systems in the absence of welldocumented exogenous antioxidant delivery

The effect and underlying mechanisms of titanium dioxide nanoparticles on glucose homeostasis: A literature review.

Titanium dioxide (TiO2 ) is used extensively as a white pigment in the food industry, personal care, and a variety of products of everyday use. Although TiO2 has been categorized as a bioinert material, recent evidence has demonstrated different toxicity profiles of TiO2 nanoparticles (NPs) and a potential health risk to humans. Studies indicated that titanium dioxide enters the systemic circulation and accumulates in the lungs, liver, kidneys, spleen, heart, and central nervous system and may cause oxidative stress and tissue damage in these vital organs. Recently, some studies have raised concerns about the possible detrimental effects of TiO2 NPs on glucose homeostasis. However, the findings should be interpreted with caution due to the methodological issues. This article aims to evaluate current evidence regarding the effects of TiO2 NPs on glucose homeostasis, including possible underlying mechanisms. Furthermore, the limitations of current studies are discussed, which may provide a comprehensive understanding and new perspectives for future studies in this field.