Brain cell alterations suggesting premature aging induced by dietary deficiency of vitamin B6 and/or copper.

Weanling albino rats were fed semisynthetic diets deficient or sufficient in vitamin B6 or copper, or both, for 2 or 3 months. Brains were examined by light and electron microscopy after Golgi impregnation or conventional tissue processing for electron microscopy. Golgi impregnation revealed that some pyramidal cells of the cerebral cortex, particularly in layers III and V, showed partial to nearly complete dendritic loss. This occurred in all deficient groups but was most typical of deficiency of vitamin B6. Swelling in dendrites or perikarya was more typical of copper deficiency. Ultrastructural observation revealed large vacuoles in cellular processes of the cerebral cortex in deficient groups. The hippocampus of copper-deficient rats contained dark, apparently degenerating processes while axonal swellings were seen in vitamin B6 deficiency. These abnormalities are discussed as evidence for accelerated aging of neurons related to poor nutritional status.

Zinc secretion in the oviduct of the coturnix quail.

The oviduct from laying quail were used to investigate mechanisms of trace mineral secretion and the possible role of metallothionein in this process. Secretion of zinc occurred maximally at pH 5.4, which is close to the normal pH of the oviduct. Secretion occurred to a much greater extent in the isthmus and shell gland than in the magnum, the major protein-secretory section of the oviduct. Intraperitoneal administration of cadmium resulted in a marked reduction in Zn secretion from the oviduct of laying quail. This effect could not be correlated with metallothionein since metallothionein could not be detected in any section of the oviduct in control or Cd-induced quail. Small-molecular-weight metal-binding ligands were present in the isthmus and shell gland, which may play a role in trace mineral mobilization. Histological evaluation by light and elelctron microscopy show that Zn is transported from the smooth muscle cells through the connective tissue matrix in the extracellular space to the epithelial goblet cells. Presumably, Zn and other trace minerals are secreted from the secretory goblet cells into the egg.

Disruption of endoplasmic reticulum is the primary ultrastructural lesion of the pancreas in the selenium-deficient chick.

Severe uncomplicated selenium (Se) deficiency was produced in chicks by feeding, from 1 day of age, a purified diet that contained 0.010 ppm Se but was adequate with respect to all other known nutrients. The deficiency was characterized by depressions in rate of growth and efficiency of feed utilization and by reductions in the plasma activity of Se-dependent glutathione peroxidase (SeGSHpx) by 85-97% from levels in chicks fed the basal diet supplemented with 0.20 ppm Se as Na2SeO3. Histological observations of the target organ of Se deficiency in the chick, i.e., the pancreas, using transmission electron microscopy, showed severe losses of endoplasmic reticulum (ER) and absence of secretory granules in acinar cells of Se-deficient animals. These effects were not uniform within individuals, as Se-deficient pancreases also showed areas of unaffected acini. By 14 days of age, Se-deficient pancreases contained many apparently undifferentiated cells, which were absent from pancreases of Se-fed chicks. It is noteworthy that abnormal mitochondria were not observed in any pancreas sections. It is concluded that the metabolic consequences of severe uncomplicated Se deficiency in the chick result from the disruption of ER and loss of functional acinar cells, rather than to damage to mitochondria as previously suggested.

Malignant mesenchymoma. Case report with electron microscopic study.

A malignant tumor from the thigh of a 65-year-old man was examined by light and electron microscopy. The tumor was diagnosed by light microscopy as malignant mesenchymoma with prevalence of leiomyosarcomatous or liposarcomatous components, but electron microscopic study revealed that the basic cell was similar to chondroblastic or osteoblastic cells. However, a precise ultrastructural classification of the tumor cells was not possible, since the majority of the cells had mixed features. The histogenesis, differentiation, and relation to prognosis are discussed.

Glomerular charge and urinary protein excretion: effects of systemic and intrarenal polycation infusion in the rat.

To study the role of the fixed anionic sites of the glomerular capillary wall in protein filtration, the negative charges were neutralized in vivo. With systemic infusion of the polycation protamine sulfate, glomerular staining for polyanion was reduced and protein excretion increased by 154%. To avoid systemic side effects in subsequent studies, small doses of a polycation were infused directly into one renal artery. The contralateral kidney was infused with the vehicle solution. Albumin excretion from the experimental kidneys in the first 1-hr collection after infusing 0.5 mg protamine sulfate was 24.3 +/- 6.3 micrograms/min/kidney (N = 13; P less than 0.01). Albuminuria declined during the subsequent 3 hr with a second infusion inducing a second proteinuric response. The degree and longevity of the albuminuric response was correlated directly to the dose of protamine sulfate. The polycations hexadimethrine and poly-l-lysine also induced proteinuria. The increased protein excretion consisted of albumin; the excretion of nonalbumin protein was identical in the experimental and control kidneys. Hemodynamic factors did not explain the increase in proteinuria. Morphologically, the polycation-treated kidneys showed scanty foot process fusion and a decrease in free negative sites in the lamina rarae of the glomerular basement membrane. The results strongly support an important role for glomerular charge in preventing filtration of circulating plasma albumin.

Diagnostic evaluation of adult polycystic kidney disease in childhood.

Since adult polycystic kidney disease, an autosomal-dominant disease, results in renal failure in at least 50% of affected patients, its detection before childbearing age is desirable. To evaluate this capability and the preferred screening technique, 28 members of two generations of an affected kindred were studied. Sonograms, excretory urograms with nephrotomograms, and clinical laboratory evaluation were compared. Five of six studied members of the older generation had cysts demonstrated by both sonograms and excretory urograms with nephrotomograms. Eleven of 22 members of the younger generation were affected, the youngest being 5 years old. In this group, excretory urograms with nephrotomograms were a slightly more sensitive detector, especially in the younger patients. However, sonography provided sufficient sensitivity in the older child, and, because of its noninvasive nature, was the preferred screening technique. The clinical laboratory evaluation was of little diagnostic aid in children with adult-type polycystic disease.