Immunolocalization of glutathione-peroxidase (GSH-PO) in human adrenal gland--studies on adrenocortical adenomas associated with primary aldosteronism and Cushing's syndrome.
Immunocytochemical localization of glutathione-peroxidase (GSH-PO) in human adrenal glands was studied on adrenocortical adenomas associated with primary aldosteronism and Cushing's syndrome. Normal adrenal glands were obtained from non-adenomatous regions of the same surgical specimens. In the normal adrenal glands, GSH-PO was immunohistochemically localized in the zonae fasciculata and reticularis of the adrenal cortex. In immunoelectron microscopic investigations, GSH-PO was localized not only in cytoplasm (cytosol GSH-PO) but also in mitochondria (mitochondrial GSH-PO). Mitochondrial GSH-PO was mostly observed in lipid-depleted inner fasciculata cells. Cytosol GSH-PO was mainly localized in lipid-laden or lipofuscin granule-laden zona reticularis cells. In the adrenocortical adenoma cells associated with primary aldosteronism, GSH-PO was weak or negative. In immunoelectron microscopic investigations, GSH-PO was localized in cytoplasm near the lipid droplets. Mitochondrial GSH-PO was hardly seen. Based on our findings, cytosol GSH-PO may play an important role in protective effects against cell injury by lipid peroxides induced in the process of the steroid hormone synthesis or the cellular aging process, and mitochondrial GSH-PO was strongly suggested to be one of the most important enzymes for steroidogenesis, especially cortisol synthesis. Furthermore, the lipid peroxidation rate in the process of aldosterone synthesis may be less than that during cortisol synthesis. In the adrenocortical adenoma cells associated with Cushing's syndrome, GSH-PO was localized mainly in lipid-depleted compact cells. Intracellular localization of GSH-PO w2s observed only in cytoplasm near the well-developed smooth endoplasmic reticulum or round mitochondria. This suggests that the intramitochondrial lipid peroxidation rate is less in the adrenocortical adenoma cells than in the normal adrenocortical cells. Furthermore, intramitochondrially derived free radicals might be diffuse across the mitochondrial membrane, and cytosol GSH-PO may be enhanced as a result. These findings may correspond to the functional significance of the adrenocortical adenoma cells.
Murakoshi
M
M
Safety Research Department, Teikoku Hormone Mfg. Co., Ltd., Kawasaki, Japan.
Osamura
R Y
RY
Yoshimura
S
S
Watanabe
K
K
D000236:Adenoma / Q000150:complications / Q000201:enzymology* / Q000473:pathology; D000306:Adrenal Cortex Neoplasms / Q000150:complications / Q000201:enzymology* / Q000473:pathology; D000311:Adrenal Glands / Q000201:enzymology* / Q000473:pathology; D000328:Adult; D003480:Cushing Syndrome / Q000150:complications / Q000201:enzymology* / Q000473:pathology; D005260:Female; D005979:Glutathione Peroxidase / Q000032:analysis*; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications / Q000201:enzymology*; D007150:Immunohistochemistry; D008297:Male; D016253:Microscopy, Immunoelectron; D008875:Middle Aged
D005979:Glutathione Peroxidase