[Structural-metabolic manifestations of the cardiotoxic effect of EDTH].
Rat myocardia exposed to 4-month inhalation of ethyl ether of 3,3-dimethyl-4,4,6-trichloro-5-hexanoic acid were studied by biochemical, morphometrical, and ultrastructural stereological methods. Long-term contact with the agent was shown to lead to myofilament regeneration impairment, resulting in a decrease in the volume density of contractile structures and in atrophy of some cardiomyocytes, which remained within 7 months of postexposure. Parallel to myofibrillar destructive alterations, there was an activation of the energy-generating compartment, which reached its maximum 1 month following the experiment and followed by mitochondrial alterations and lower SDH activity. It is concluded that the degenerative changes in cardiomyocytes are primarily associated with the functional overload and depletion of mitochondrial resources.
Sarbaeva
N N
NN
Balueva
O B
OB
Miliakova
M N
MN
Kaz'mina
N P
NP
D000818:Animals; D001284:Atrophy; D005229:Fatty Acids, Monounsaturated / Q000633:toxicity*; D006321:Heart / Q000187:drug effects*; D008929:Mitochondria, Heart / Q000201:enzymology / Q000473:pathology; D009206:Myocardium / Q000201:enzymology / Q000473:pathology* / Q000648:ultrastructure; D010575:Pesticides / Q000633:toxicity*; D051381:Rats; D013385:Succinate Dehydrogenase / Q000378:metabolism
D005229:Fatty Acids, Monounsaturated; D010575:Pesticides; C076766:3,3-dimethyl-4,6,6-trichloro-5-hexenic acid ethyl ester; D013385:Succinate Dehydrogenase
Strukturno-metabolicheskie proiavleniia kardiotoksicheskogo éffekta EDTG.