title: Myopathy: a possible effect of chronic low level lead exposure.
abstract: Morphological changes in the central nervous system and other organs have been reported in numerous studies investigating low level lead exposure. To date, however, there are no investigations on the effect of low level lead exposure on striated muscles, although varying neuromuscular changes in different species have been known for years. Rhesus monkeys were exposed pre- and postnatally to lead acetate in the diet (350 ppm or 600 ppm) over 9 years, followed by a lead free period of 32 months, while a control-group received regular diet. No signs of muscular dysfunction were evident. To elucidate neuromuscular pathomorphology frozen sections of the vastus medialis muscle were processed for routine and enzymohistological staining (Hematoxilin and Eosin, Sudan Black, Gomori, NADH, ATPase). Resin histology was processed for electron microscopy. Morphometric analysis was made with commercial software. Light microscopy revealed dose-related signs of myopathy in the lead-exposed groups. The scatter of fibre diameters was increased, and split fibers and internal nuclei were more frequent. Fibres became separated from each other by copious endomysial connective tissue. Ultrastructural examination showed hydropic mitochondria and a massively dilated sarcotubular system in the 600 ppm group. Dose-related extracellular collagen deposition increased. A heavy fibrosis was seen in the 600 ppm group. These findings are interpreted as myopathical reaction due to chronic low level lead exposure, as there were no signs of neurogenical lesion. It remains unknown how the fibrosis developed. A primary fibrosis could be based upon a developmental delay of satellite cells (expressing metalloproteases for collagen-catabolism). Lead is known to inhibit regular development in many ways if exposure has started prenatally. As the skeletal muscle is a common target of toxicity, the myotoxic effects of chronic low level lead exposure comes into question.
authors.affiliation: Neurologische Klinik und Poliklinik, Universitätsklinikum Charité, Humboldt-Universität Berlin, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Buchheim
authors.forename: G
authors.initials: G
authors.lastname: Stoltenburg-Didinger
authors.forename: H
authors.initials: H
authors.lastname: Lilienthal
authors.forename: G
authors.initials: G
authors.lastname: Winneke
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002908:Chronic Disease; D005260:Female; D007855:Lead Poisoning / Q000473:pathology*; D008253:Macaca mulatta; D008297:Male; D008854:Microscopy, Electron; D018485:Muscle Fibers, Skeletal / Q000473:pathology / Q000648:ultrastructure; D018482:Muscle, Skeletal / Q000473:pathology / Q000648:ultrastructure; D009135:Muscular Diseases / Q000139:chemically induced* / Q000473:pathology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects