Disruption of brain mitochondrial calcium sequestration by methylmercury. j

In vitro effects of methylmercury (MeHg) on Ca2 transport and respiratory control of mitochondria isolated from rat forebrain were examined to determine whether MeHg disrupted seques-tration of Ca2 by neuronal mitochondria. Uptake of 45Ca2 by mitochondria and release of 45Ca2 from preloaded mitochondria were measured in the presence and absence of ATP. Release of 45Ca2 from preloaded mitochondria by MeHg was measured in the presence and absence of ruthenium red (RR), a putative inhibitor of the mitochondrial Ca2 uptake uniporter. During in-cubation intervals ranging from 1 0 sec to 5 mm, 1 0 M MeHg reduced mitochondnal uptake of 45Ca2 by about 50 % and 100 zM MeHg completely prevented 45Ca2 uptake. These effects of MeHg occurred in both the presence and absence of ATP. Exposure of mitochondria preloaded with 45Ca2 to either 1 0 t