Objective
To investigate the effects of acute and subacute exposures to different doses of lead acetate on lead distribution in mice.
Methods
This study included acute and subacute lead exposure experiments. As for the acute lead exposure experiment, fifteen male ICR mice were randomly divided into control group, low-lead group, and high-lead group, with five mice in each group. The low-lead group and the high-lead group were given lead acetate solution (25 and 100 mg/kg) through intraperitoneal injection, while the control group was injected with equal volume of normal saline. All mice were sacrificed to collect samples at 24 h after exposure. As for the subacute lead exposure experiment, thirty male ICR mice were randomized into control group (reverse osmosis water), low-lead group (250 mg/L lead acetate solution), and high-lead group (2 500 mg/L lead acetate solution), with 10 mice in each group. Samples were collected after the mice were exposed to lead through drinking water for 28 d. For the two experiments, samples of serum, blood cells, testis, heart, liver, lung, kidney, and brain were collected from mice, and organ weights were measured. All samples were fast frozen in liquid nitrogen and stored in a -80℃ refrigerator for later detection. Graphite furnace atomic absorption spectrophotometry was used to measure lead concentration in all samples. Analysis of variance and rank test were used to analyze the experimental data.
Results
The results from the acute lead exposure experiment showed that the low-dose and the high-dose lead treatment significantly increased lead levels in serum (by 7.7 and 32.2 times), blood cells (by 4.4 and 7.0 times), lung (by 21.8 and 43.3 times), liver (by 75.0 and 230.2 times), kidney (by 14.3 and 40.3 times), and testis (by 13.0 and 20.3 times) of mice as compared to the controls, respectively (P < 0.05). The high-dose lead treatment further increased lead levels in heart (by 0.9 times, P < 0.05) of mice, but did not cause obvious changes in lead levels in brain (P>0.05). Different doses of lead treatment did not result in body weight changes in the mice (P>0.05). Only the low-dose lead treatment caused a decrease in the ratio of lung to body weight (P < 0.05). The results from the subacute lead exposure experiment showed that the lead levels in lung (by 1.7 and 3.0 times), liver (by 51.4 and 107.5 times), kidney (by 4.7 and 19.7 times), and brain (by 1.9 and 7.2 times) of mice was increased by low-dose and high-dose lead exposure via drinking water as compared to the controls, respectively. The high-dose lead exposure also significantly elevated the levels of lead in serum (by 0.4 times), blood cells (by 5.3 times), heart (by 2.3 times), and testis (by 2.0 times) of mice, reduced the drinking water consumption of mice (P < 0.05), but had no effect on body weight and diet intake. The low-dose lead exposure increased the ratio of heart to body weight (P < 0.05), whereas the high-dose lead exposure reduced the ratio of liver to body weight (P < 0.05).
Conclusion
Under the experimental conditions, both acute and subacute lead exposures cause accumulation of lead in lung, liver, and kidney of mice. Moreover, acute lead treatment induces lead accumulation in mouse testes, and subacute lead exposure results in lead accumulation in mouse brain.
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