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675308 
Journal Article 
Mitochondrial toxicity of phthalate esters. Conference pn phthalates, Washington, D.C., June 
Melnick, RL; Schiller, CM 
1981 
Yes 
Environmental Health Perspectives
ISSN: 0091-6765
EISSN: 1552-9924 
45 
0 
51-56 
The effects of phthalate esters on rat liver mitochondrial energy coupling and electron transport were studied. Preparations of liver mitochondria from male CD-rats were incubated with various concentrations of mono-n-butyl-phthalate (131704) (MBP), di-n-butyl-phthalate (84742) (DBP), mono(2-ethylhexyl)-phthalate (4376209) (MEHP), or di(2-ethylhexyl)-phthalate (117817) (DEHP). Changes in energy dependent potassium ion (K+) uptake, respiration rates, and succinate cytochrome-c reductase activity were measured. Energy linked K+ uptake was most strongly inhibited by DBP and MEHP, while DEHP had no effect. Both DBP and MEHP acted as potent uncouplers of oxidative phosphorylation and inhibitors of succinate oxidation; MBP was moderately potent, and DEHP was inactive. Succinate cytochrome-c reductase activity was most strongly inhibited by MEHP, significantly inhibited by DBP and unaffected by MBP or DEHP. The authors conclude that phthalate esters affect isolated rat liver mitochrondria by uncoupling energy linked processes and by inhibiting succinate dehydrogenase activity. The compounds alter the permeability properties of the inner cell membrane. Phthalate induced peroxisome proliferation may be a result of cellular response to inhibition of mitochondrial succinate oxidation, while hypolipemia may arise partly from reduced lipid biosynthesis caused by decreased mitochondrial adenosine-triphosphate synthesis or increased oxidation due to loss of respiratory control. 
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