Effects of lead on mice protein synthesis in vivo and in vitro

Abstract

Objective: To evaluate effects of lead ions on the general protein synthesis in mouse organs in vivo and in liver cell-free translation system. Methods: Experiments were done on white laboratory mice using i.p. injections of appropriate amounts of lead acetate solution. Protein synthesis was evaluated by the incorporation of 14 C-labeled leucine into newly synthesized proteins. Liver cell-free translation system was made on the basis of post-mitochondrial supernatant. Results: Even a sublethal concentration of lead ions (0.5 LD 50 ) was not capable to yield major protein synthesis inhibition in mouse liver, kidneys, skeletal muscle and heart 24 h after the experimental intoxication. Further increase of lead ions up to 0.75 LD 50 significantly decreased protein synthesis in these organs (except the liver). However, we found that at earlier stages of intoxication (within initial 8 h), strong perturbations of protein synthesis occur in mouse organs; 0.5 LD 50 lead caused a significant stimulation of translation in liver and kidneys, which reached 202% in liver at 8th h and 175% in kidneys at 2nd h. Protein synthesis in skeletal muscle was both stimulated by 43% at 2nd h and suppressed by 36% at 8th h. Lead ions did not cause any severe fluctuations in the heart translation intensity; 48 h after the experimental intoxication protein synthesis in studied organs was as in norm. Data of experiments in vitro showed that lead ions at concentration up to 50 pM activate translation in liver cell-free protein-synthesizing system. This concentration is approximately 10-fold lower than that one needed to obtain stimulatory effect in vivo. Conclusions: Lead ions induce significant fluctuations of protein synthesis activity at the early stages of intoxication in vivo, which tend to become normalized with time. Lead at low concentration is capable to stimulate protein synthesis both in vivo and in vitro.