Related Experiment Video
Updated: Aug 7, 2026
Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Influence of selenium treatment on the acute toxicity of dibutyltin dichloride in rats
Background/Aims:
Dibutyltin dichloride (DBTC) is an organotin compound used as a model for acute pancreatitis. The aim was to determine the effect of various doses of Na-selenite on the pathogenesis and course of DBTC-induced toxic changes in organs and serum of rats.
Methods:
Experimental pancreatitis was induced by intravenous administration of 6 mg kg(-1) BW DBTC. Na-selenite was applied as a single intravenous dose of 5 mg kg(-1) BW and as daily oral dose of 1 mg kg(-1) BW. Malondialdehyde (MDA) was detected to observe the level of oxidative stress. The tin concentration in bile and urine shows the elimination of DBTC. Organ changes were indicated by serum parameters as well as histology.
Results:
DBTC causes an acute pancreatitis, cholestasis and liver lesions determined by specific elevated serum parameters and several histological lesions. Na-selenite significantly diminished MDA concentration, lipase, bilirubin and transaminases as well as organ injuries compared to only DBTC-treated rats.
Conclusions:
The treatment with Na-selenite in the scope of DBTC-induced pancreatitis points to a reduced oxidative stress characterized by diminished MDA serum levels and a milder course of pancreatitis. The generation of DBTC-Na-selenite complexes could also be a mechanism to decrease the toxicity of organotin compounds like DBTC.
Insights
Sodium selenite (Na-selenite) treatment reduced oxidative stress and pancreatitis severity in rats exposed to dibutyltin dichloride (DBTC). This suggests Na-selenite may mitigate organotin compound toxicity.
Area of Science:
- Toxicology
- Biochemistry
- Pathology
Background:
- Dibutyltin dichloride (DBTC) is an organotin compound utilized as an experimental model for acute pancreatitis.
- DBTC exposure induces toxic changes in rat organs and serum, mimicking pancreatitis pathogenesis.
Purpose of the Study:
- To investigate the therapeutic effects of varying doses of sodium selenite (Na-selenite) on DBTC-induced pancreatitis.
- To evaluate Na-selenite's impact on oxidative stress markers and organ damage in rats.
Main Methods:
- Acute pancreatitis was induced in rats via intravenous administration of DBTC.
- Na-selenite was administered intravenously or orally at different dosages.
- Oxidative stress was assessed by measuring malondialdehyde (MDA) levels.
- DBTC elimination was monitored by measuring tin concentration in bile and urine.
- Serum parameters and histological examination were used to evaluate organ damage.
Main Results:
- DBTC induced acute pancreatitis, cholestasis, and liver lesions, evidenced by elevated serum markers and histological changes.
- Na-selenite treatment significantly reduced MDA concentration, serum lipase, bilirubin, and transaminases.
- Na-selenite administration attenuated DBTC-induced organ injuries compared to control groups.
Conclusions:
- Na-selenite treatment effectively reduces oxidative stress, indicated by lower MDA levels, and ameliorates the severity of DBTC-induced pancreatitis.
- The formation of DBTC-Na-selenite complexes may represent a key mechanism for decreasing the toxicity of organotin compounds.
