Paradoxical effect of methyl mercury on mitochondrial protein synthesis in mouse brain tissue.
The intraperitoneal administration of a single dose of methyl mercuric chloride (MeHg) (10 or 50 nmol/g body weight) to adult male mice led to a significant stimulation of protein synthesis directed by isolated brain mitochondria in a special cell-free translation system prepared from rabbit reticulocyte lysates. The pre-treatment of the isolated mouse brain mitochondria from MeHg-injected and control (saline-injected) animals with an inhibitor (oligomycin) or inducers (ADP, succinate) of ATP synthesis showed that mitochondrial translation activity was high when ATP synthesis was suppressed and low when ATP synthesis was stimulated.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008767:Methylmercury Compounds / Q000633:toxicity*; D051379:Mice; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000096:biosynthesis* / Q000235:genetics; D009840:Oligomycins / Q000494:pharmacology; D014176:Protein Biosynthesis; D011691:Puromycin / Q000494:pharmacology; D011817:Rabbits; D012156:Reticulocytes / Q000378:metabolism; D013386:Succinates / Q000494:pharmacology
D008767:Methylmercury Compounds; D009419:Nerve Tissue Proteins; D009840:Oligomycins; D013386:Succinates; D011691:Puromycin; D000244:Adenosine Diphosphate; C004925:methylmercuric chloride