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Pulmonary toxicity of systemic terbium chloride in mice
H Shimada1, M Nagano, T Funakoshi
1Department of Hygienic Chemistry, Faculty of Pharmaceutical Sciences, Kumamoto University, Japan.
Abstract:
Terbium (Tb) is a rare earth metal that finds use in several emerging technologies. However, little is known about the biological effects of Tb. Thus, in this study the pulmonary toxicity of systemic Tb in mice was investigated. Mice were treated intravenously with a single dose of 20 or 200 mumol Tb/kg, as TbCly and killed at 3, 6, 12, 24, 48, or 72 h later. Administration of Tb at a dose of 200 mumol/kg increased pulmonary weight, lipid peroxidation, and protein content but decreased pulmonary glutathione content. Pulmonary gamma-glutamyl transpeptidase (gamma-GTP) activity was increased after Tb administration at a dose of 200 mumol/kg. Pulmonary alkaline phosphatase (ALP) activity was also increased after Tb administration at a dose of 200 mumol/kg. Investigation of the defense system against oxidative damage in the lung showed that superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were all decreased after Tb administration at the higher dose. The concentrations of Tb, Ca, and P in lung was increased by the dose of 200 mumol/kg. These results suggest that pulmonary lipid peroxidation may be an early and sensitive consequence of Tb exposure and that SOD, CAT, and GSH-Px might be considered as potential modulators of Tb-induced lipid peroxidation. The mechanisms involved in Tb-induced pulmonary lipid peroxidation deserve further study.
Insights
Terbium (Tb) exposure in mice caused lung damage, increasing lipid peroxidation and decreasing antioxidant defenses. These findings highlight the pulmonary toxicity of this rare earth metal.
Area of Science:
- Environmental Toxicology
- Materials Science
- Biochemistry
Background:
- Terbium (Tb), a rare earth metal, is increasingly used in technology.
- Limited data exists on the biological impacts of Tb exposure.
- Understanding Tb's toxicity is crucial for occupational and environmental safety.
Purpose of the Study:
- To investigate the pulmonary toxicity of systemic Terbium (Tb) exposure in a mouse model.
- To assess the effects of Tb on lung oxidative stress markers and enzyme activities.
- To identify potential mechanisms underlying Tb-induced lung injury.
Main Methods:
- Mice received single intravenous doses of Terbium chloride (TbCl3) at 20 or 200 µmol/kg.
- Pulmonary toxicity was evaluated at various time points (3-72 hours) post-administration.
- Measurements included lung weight, lipid peroxidation, protein content, glutathione levels, and enzyme activities (gamma-GTP, ALP, SOD, CAT, GSH-Px).
- Terbium, calcium, and phosphorus concentrations in lung tissue were quantified.
Main Results:
- A high dose (200 µmol/kg) of Tb significantly increased lung weight, lipid peroxidation, and protein content.
- Glutathione content in the lungs decreased following Tb administration.
- Activities of key antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), were reduced.
- Pulmonary gamma-glutamyl transpeptidase (gamma-GTP) and alkaline phosphatase (ALP) activities were elevated.
- Lung concentrations of Tb, calcium (Ca), and phosphorus (P) increased significantly at the higher dose.
Conclusions:
- Pulmonary lipid peroxidation is an early and sensitive indicator of Terbium exposure.
- Terbium exposure impairs the lung's antioxidant defense system, evidenced by decreased SOD, CAT, and GSH-Px activities.
- Further research is warranted to elucidate the mechanisms of Terbium-induced pulmonary lipid peroxidation and its modulators.