Regulation of lipid peroxidation in the retina under the effect of bright light.

Changes in LPO intensity under the effect of exposure to bright light and the possibility of their correction with antioxidants were studied on rabbits with diabetic retinopathy. It was found that enhanced LPO caused by exposure to bright light in rabbits with diabetic retinopathy can be corrected with antioxidants. Phenosan potassium salt, α-tocopherol, and oxypyridine were more effective than SOD and taurine in preventing MDA accumulation. A complex of natural and synthetic antioxidants was most efficient in correcting LPO under conditions of exposure to bright light.

A Paneth cell specific zinc-binding protein in the rat. Purification and immunohistochemical localization.

BACKGROUND: Paneth cells are zinc-containing cells widely distributed in Lieberkühn's crypts of small intestine in many species, but their function has remained obscure. Our previous study showed that a single intravenous injection of diphenylthiocarbazone (dithizone), a zinc chelator, forms zinc-dithizonate complexes in the cytoplasm of Paneth cells to ensure rapid and selective killing of the cells. EXPERIMENTAL DESIGN: To verify the proteins that selectively deleted from intestinal mucosa after dithizone treatment, intestinal proteins from the rats with or without dithizone injection were compared in sodium dodecyl sulfate-polyacrylamide gel electrophoresis. One such protein, a 90 kilodalton (kd) protein, was purified to homogeneity from normal rat intestine. A polyclonal antiserum was prepared by immunizing a rabbit with purified 90 kd protein to use in immunohistochemical study. RESULTS: Among several proteins deleted after dithizone injection, a 90 kd protein with an isoelectric point of 5.9 +/- 0.2, was purified to homogeneity from normal intestine by a combination of zinc affinity column and electroelution. Immunohistochemistry with rabbit anti-90 kd antiserum showed that the cytoplasmic granules in Paneth cells were stained. After dithizone administration, the 90 kd protein containing cells rapidly disappeared, but resumed as Paneth cells regenerated. Also positively stained with this antibody were a few mononuclear cells broadly distributed in the lamina propria of the digestive tract, but they were not affected by dithizone treatment. CONCLUSIONS: A 90 kd zinc-binding protein was identified and purified from rat Paneth cells that was deleted in dithizone-treated rat intestine. We propose to designate it as a zinc-binding protein of Paneth cell.

[Zinc contents of pancreatic islets in animals of various species after administration of diabetogenic agent, dithizone]. / Soderzhanie tsinka v pankreaticheskikh ostrovkakh u zhivotnykh raznykh vidov pri vvedenenii diabetogennogo agenta ditizona.

A decrease of zinc content in pancreatic islet was shown in animals which received diabetogenic agent dithizone. The changes of islet zinc content occurred mainly on account of insulin-producing cells and in coincidence with glycemia changes.

The diabetogenic and acidotropic effects of chelators.

Diabetogenic and acidotropic effects of dithizone, 8-(p-toluenesulfonylamino)-quinoline and 8-(benzenesulfonylamino)-quinoline were studied in experiments on cats, rabbits, golden hamsters and mice. Selective damage of insulin producing cells, phase glycemic fluctuations and permanent diabetes development were shown to be connected with chelator zinc binding in the lysosome-segregation apparatus of these cells.

Zinc distribution in mouse brain subsequent to hippocampal lesions.

The role of zinc in central nervous system metabolism remains obscure but it has been shown in animals that diphenylthiocarbazone (Dithizone) selectively colors intravitally the hippocampus and adnexa, parts affected in human temporal lobe epilepsy. To examine the effect of experimental cerebral lesions on zinc storage in that region, 80 mice were divided into two operative and two control groups. The operative groups had unilateral lesions placed in the hippocampus or frontal lobe. One control group and both lesion groups were injected subcutaneously with zinc lactate daily for ten days before intravenous injection of diphenylthiocarbazone. The other control group was used to determine if zinc storage occurs as a result of its increased systemic availability. Hippocampal lesion mice showed more extensive staining of lethal amygdala and associated cortex on the side of the lesion. Frontal lesions remained unstained and frontal lesions did not alter the staining of hippocampus and related parts. Lack of difference between controls shows that greater availability of systemic zinc does not increase its content in the hippocampal-lateral amygdalar region. Increased zinc uptake in this instance appears to be a local phenomenon.