To evaluate the ultrastructural changes and the mechanism causing liver injury by lead, light and electron microscopic(LM and EM) examination using Timm sulphide silver method(TSM) was done. Sprague-Dawley rats were divided into a control and 3 experimental groups. The experimental groups were orally administered 0.5% lead acetate(LA). Group 1 received a one time dose of 10 ml of LA by gastric intubation. Groups 2 and 3 continuously received LA instead of drinking water. The control group was composed of 3 rats in each group which did not receive any treatment. Rats of group 1, 2 and 3 and control were sacrificed at 1/2, 1, 1 1/2 hours, 2 days, and at 1, 2, 4, 6 and 8 weeks later, except group 3. Before sacrifice, they were perfused with 0.1% sodium sulphide and 2.5% glutaraldehyde through the abdominal aorta for TSM. The liver was taken for LM and EM examinations. Blood lead concentration began to increase from the 2nd day up to 3.29 microgram/ml at 2nd week, and the urinary delta-ALA level showed a steady increase from the 2nd day. LM and EM examination of liver revealed that absorbed lead granules in group 1 were transported into sinusoidal spaces, Kupffer cells, and the hepatocytes within 1 hour and then disappeared 1/2 hour thereafter. In group 2 deposited lead was found in the hepatocytic cytosol bound to mitochondria. That in turn inhibited mitochondrial respiration with resultant mitochondrial swelling at the 1st week and thereafter at 6th week myelin figure formation and condensation of mitochondria, and peroxisomes were increased at 8th week. Based on these results it can be concluded that a transient intake of subletal dose of LA is biotransformed completely by periportal hepatocytes within 1 1/2 hours, but excessively accumulated lead can induce liver cell injury due to lipid peroxidation of membrane by direct toxic effect of lead and by products of lipid peroxidation. We postulate that lead acetate triggers presumably primarily mitochondrial membrane injury and then other organellar changes may play a role in disturbance of a network of interacting of key events capable of causing cell death.
Rats ; Animals

No abstract available.
Hip* ; Natural History* ; Technetium Tc 99m Medronate*

No abstract available.
Gonadotropin-Releasing Hormone* ; Gonadotropins*

An eccrine squamous syringometaplasia (ESS) is defined as a mature squamous metaplasia of the eccrine ducts. The clinical and pathological features of an ESS are presented. Syringometaplasia is a rare lesion, mostly occuring in the extremities, and as far as we know, no report on the ESS has been published in Korean literature. We experienced a case of an ESS occured in a 15 year-old male, who had a tender erythematous plaque in the right knee. The histologic examination revealed some scattered nests of metaplastic squamous epithelium in the deep dermis, associated with acute nonspecific panniculitis. The importance of the ESS is that it histologically simulates the well differentiated squamous cell carcinoma. The histopathologic findings were discussed and a brief review of the literature was made.
Adolescent ; Carcinoma, Squamous Cell ; Dermis ; Epithelium ; Extremities ; Humans ; Knee ; Male ; Metaplasia ; Panniculitis

No abstract available.
Embryo Transfer* ; Embryonic Structures* ; Fertilization in Vitro* ; Pregnancy*

No abstract available.
Female ; Humans ; Pregnancy ; Pregnancy Trimester, Second* ; Pregnancy*

No abstract available.
Pregnancy*

No abstract available.
Oocyte Donation* ; Oocytes*

No abstract available.
Fertilization* ; Oocytes*

No abstract available.
Fertilization in Vitro* ; Superovulation*