Exp. Pathol. 1991; 43: 247-250 Gustav Fischer Verlag Jena Short Communication

University of Chicago, School of Medicine, Department of Pathology, Chicago, U.S.A. and Karolinska Institute, Stockholm, Sweden

Effect of pyridoxine deficiency on the adrenal cortex

S. A. G. DATSIS

With 3 figures

Received: March 21, 1990; Accepted: April 18, 1990

Address for correspondence: Dr. med. S. A. G. DATSIS, 31 Aristotelus Street, 54631 Thessaloniki, Greece

Key words: adrenal cortex; pyridoxine deficiency; autophagic vacuoles; zona fasciculata; desoxypyridoxine

Malnutrition has been shown to effect a modification in structure an function of endocrine glands (JACKSON 1925, 1929). In the rat, adrenal hypertrophy is associated with a deficiency of cartain factors of the vitamin "B" complex, such as thiamine and pantothenic acid (DEANE 1946).

The method for creating the cellular challenge for the pyridoxine depletion experimental system is careful exclusion from an otherwise normal diet by the use of a standard pyridoxine­free commercial diet preparation (General Biochemicals) and tap water. Ad libitum feeding follows a preliminary period of 8 h fasting. At appropriate intervals after the initiation of the pyridoxine-free feeding, tissue samples from the adrenal cortex may be obtained for electron microscopic analysis.

The adrenal cortical cytoplasmic change characterizing this experimental system is a tissue reaction that affects all adreno-cortical parenchymal cells. Significant enlargement of the adrenal gland of pyridoxine-depleted rats, predominantly involving the zona fasciculata is observed when severe pyridoxine deficiency is enhanced with the vitamin antagonist desoxy­pyridoxine. This effect of pyridoxine deprivation is not a consequence of caloric restriction.

The microscopic appearance of the adrenal cortex is greatly altered in pyridoxine deficiency. The zona fasciculata shows a progressive loss to the point of extinction of sudanophilic lipoid, birefringent material and cholesterol.

Ultrastructural studies on the adrenal cortex of pyridoxine depleted rats further clarified the morphologic basis for the formation of the dense, osmiophilic droplets occurring in the cytoplasm of the cells of the zona fasciculata and to a lesser extent of the glomerulosa and reticularis. Evidence indicates that ultrastructural alterations indicative of a physiologic autolysis of the cytoplasm, probably as an expression of a high metabolic activity and rapid turnover of the cytoplasm accompany pyridoxine deficiency. An extensive involvement of mitochondria and the ergastoplasm in the autolytic process is seen to occur. The formative stages of the autophagic vacuoles and of the subsequent residual bodies seem to involve the wrapping of a flattened sac made-up of smooth and/ or rough surfaced membranes, around a small area of the cytoplasm (figs. 1, 2, 3). The origin of the membrane forming the sac is not

Exp. Pathol. 43 (1991) 3-4 247

Fig. 1. Electron micrograph showing part of the cytoplasm of a zona fasciculata cell from a 4-day depleted rat. Gradual disorganization of the internal mitochondrial structure leading to the formation of autophagic vacuoles, eventually giving rise to residual bodies is clearly depicted. Fixation in 6.25 % glutaraldehyde in phosphate buffer, postfixation in 1 % OS04, and stained with uranyl acetate and leda hydroxide. X 22,000. Abbr.: L=lipid droplet, M=mitochondrion, Av=autophagic vacuole, Db=dense body.

Figs. 2, 3. Survey electron micrographs showing the gradual loss in the mitochondrial internal structure, the formation of cytosegresomes and/ or autophagic vacuoles as well as of dense bodies. A vesiculation of the ergastoplasm with an apparent increase in the number of free ribosomal profiles are noticeable. X 22,000. Fixation and staining as in fig. 1. Abbr. : erg. = ergastoplasm, rb = ribosomes, ill = mitochondrion, Cs = cytosegresome, Av = auto­phagic vacuole.

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Exp. Pathol. 43 (1991) 3-4 249

clear, but the appearance suggests the Golgi lamellae or the endoplasmic teticulum as possible sources.

A marked disorganization of the membranous component of the mitochondria comprises the primary stages in the formation of the majority of the myeloid bodies. These changes, accompanied by a moderate densification of the mitochondrial matrix, cause a progrediating obliteration of the mitochondrial structure. Numerous cells also possess swollen mitochondrial profiles with a scant internal structure.

The formation of dilated cisternae of the ergastoplasm is frequently depicted. A prominent dilatation of the smooth surfaced endoplasmic reticulum, assuming a vesicular appearance also comprises a major part of the ultrastructural appearance. An apparent increase in the number of free ribosomes throughout the entire cortical area accompanies the overall submicroscopic picture (fig. 2)

Administration of desoxypyridoxine accelerates the appearance of the deficiency symp­toms and the morphological alterations in the adrenal cortex. Comparable inanition produced no significant changes in the adrenal cortex. Thus, the extensive changes observed in the cortex of the desoxypyridoxine deficient animals must be attributed to the effect of pyridoxine deprivation.

References

DEANE, H. W., McKibbon, J. M.: The chemical cytology of the adrenal cortex in pantothenic acid deficiency. Endocrinology 38: 385, 1946.

JACKSON, C. M.: The effect of inanition and malnutrition upon growth and structure. P. Blackiston Sons and Co., Philadelphia, PA, 1925. Recent work on the effects of inanition and malnutrition on growth and structure. Arch. Pathol. 19297: 1042. Recent work on the effects of inanition and malnutrition on growth and structure. Arch. Pathol. 1929; 8: 81.

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