Search research articles

Related Concept Videos

Bioactivation and Tissue Toxicity

Bioactivation and Tissue Toxicity

Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Directional Concerted Proton-Electron Transfer in COFs for Efficient Photocatalytic H<sub>2</sub>O<sub>2</sub> Production.

Advanced materials (Deerfield Beach, Fla.)·2026

Same author

Metformin-Associated Gastrointestinal Intolerance: A Narrative Review of Mechanisms and Clinical Management.

Clinical medicine insights. Endocrinology and diabetes·2026

Same author

Research progress and trends on M2 macrophages in breast cancer research: a bibliometric analysis.

Discover oncology·2026

Same author

Research progress of dengue virus T cell epitope mediated cellular immunity in avoiding ADE.

Frontiers in immunology·2026

Same author

Using the Behaviour Change Wheel framework to develop an integrated intervention for diabetes and hypertension co-management in China: a case report.

BMC global and public health·2025

Same author

Higher Controlling Nutritional Status (CONUT) score indicates increased risk of sarcopenia in elderly hospitalized patients: a single institution study in China.

Frontiers in nutrition·2025

Same journal

Parental co-exposure to polystyrene nanoplastics and cadmium primes adaptive intergenerational responses in Arabidopsis thaliana.

Journal of hazardous materials·2026

Same journal

Multi-phase fate and removal mechanism of acetamiprid in a planted coastal wetland mesocosm system: A 'dual-engine' perspective.

Journal of hazardous materials·2026

Same journal

Chronic exposure to Bisphenol AF from gestation through adulthood induces renal injury in 8-month-old mice via lipid metabolism dysregulation and ferroptosis.

Journal of hazardous materials·2026

Same journal

Characterising subsea gas pipeline contaminants to inform decommissioning practices, an ecosystem perspective.

Journal of hazardous materials·2026

Same journal

Compartment-specific host association and mobility shape ARG risk in aquaculture systems.

Journal of hazardous materials·2026

Same journal

Decoupling functional group effects on uranium adsorption in UiO-66 through density functional theory and neural network modeling.

Journal of hazardous materials·2026

See all related articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Search research articles

Related Experiment Video

Updated: Apr 27, 2026

Advanced 3D Liver Models for In vitro Genotoxicity Testing Following Long-Term Nanomaterial Exposure

Advanced 3D Liver Models for In vitro Genotoxicity Testing Following Long-Term Nanomaterial Exposure

Published on: June 5, 2020

Nano-sized titanium dioxide-induced splenic toxicity: a biological pathway explored using microarray technology.

Lei Sheng¹, Ling Wang², Xuezi Sang¹

¹Medical College of Soochow University, Suzhou 215123, China.

Journal of Hazardous Materials

|June 27, 2014

Summary

This summary is machine-generated.

Titanium dioxide nanoparticles (TiO2 NPs) cause spleen damage, immune dysfunction, and apoptosis in mice. Gene expression analysis revealed significant alterations, identifying potential biomarkers for TiO2 NP-induced splenic toxicity.

Keywords:

Gene-expressed profile Spleen injury Splenic dysfunction Titanium dioxide nanoparticles

More Related Videos

In Situ Detection and Single Cell Quantification of Metal Oxide Nanoparticles Using Nuclear Microprobe Analysis

In Situ Detection and Single Cell Quantification of Metal Oxide Nanoparticles Using Nuclear Microprobe Analysis

Published on: February 3, 2018

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro

Published on: January 31, 2022

Related Experiment Videos

Last Updated: Apr 27, 2026

Advanced 3D Liver Models for In vitro Genotoxicity Testing Following Long-Term Nanomaterial Exposure

Advanced 3D Liver Models for In vitro Genotoxicity Testing Following Long-Term Nanomaterial Exposure

Published on: June 5, 2020

In Situ Detection and Single Cell Quantification of Metal Oxide Nanoparticles Using Nuclear Microprobe Analysis

In Situ Detection and Single Cell Quantification of Metal Oxide Nanoparticles Using Nuclear Microprobe Analysis

Published on: February 3, 2018

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro

Published on: January 31, 2022

Area of Science:

Environmental Toxicology
Nanotechnology
Immunology

Background:

Titanium dioxide nanoparticles (TiO2 NPs) are widely utilized, raising concerns about their potential toxicity.
The molecular mechanisms underlying TiO2 NP-induced splenic injury remain incompletely understood.

Purpose of the Study:

To investigate the effects of TiO2 NPs on spleen immune capacity and gene expression.
To identify molecular mechanisms and potential biomarkers of TiO2 NP-induced splenic toxicity.

Main Methods:

Mice were administered varying doses of TiO2 NPs (2.5, 5, or 10 mg/kg) via intragastric administration for 90 days.
Spleen indices, immune function, and histological changes (macrophage infiltration, apoptosis) were assessed.
Microarray analysis was employed to examine gene expression profiles in damaged spleens.

Main Results:

TiO2 NP exposure led to dose-dependent increases in spleen indices, immune dysfunction, macrophage infiltration, and apoptosis.
Microarray data revealed significant alterations in 1041 genes related to immunity, inflammation, apoptosis, oxidative stress, and metabolism.
Specific genes like Cyp2e1, Sod3, Mt1, Mt2, Atf4, and Cxcl13 were identified as potential biomarkers.

Conclusions:

TiO2 NPs induce significant splenic injury, characterized by immune dysfunction and cellular damage.
Comprehensive gene expression changes highlight the molecular pathways affected by TiO2 NP exposure.
Identified genes may serve as valuable biomarkers for assessing TiO2 NP-induced spleen toxicity.