Degeneration of the rat and canine adrenal cortex caused by ?-(1,4-dioxido-3-methylquinoxalin-2-yl)-N-methylnitrone (DMNM)

Yarrington, J. T.; Loudy, David E.; Sprinkle, D. Jean; Gibson, John P.; Wright, Carol; Johnston, J.O'Neal

doi:10.1016/0272-0590(85)90085-5

Cited by 13 publications

(3 citation statements)

References 10 publications

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“…Most cells appeared swollen and distended with highly vacuolated cytoplasm. This might be owed to that adrenal cortical cells contain large stores of lipids which is the substrate for steroidogenesis as mentioned by Yarrington et al (1986). Impaired steroidogenesis can result in excess steroid precursors and cytoplasmic vacuolations (Rosol et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

The possible structural changes in the adrenal gland cortex after induction of hepatic ischemia–reperfusion injury in male albino rats: Light and electron microscopic study

El‐Tahawy

Abozaid

2019

Journal Cellular Physiology

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The adrenal gland is an important endocrine gland in the body that secrets the adrenal hormones. One of the important clinical issues is the hepatic ischemia–reperfusion (IR) injury. Liver IR injury results in many distant organs dysfunctions such as lung, kidney, intestine, pancreas, and myocardium. The aim of the present study was to investigate the possible remote effects of hepatic IR on the structure of the adrenal cortex. Twenty healthy males, Sprague–Dawley albino rats aged 6–8 weeks were randomly divided into two groups (10 rats each): the sham control group (SC‐group) and the ischemia–reperfusion group (IR‐group). Sera were estimated for the following: aspartate transaminase (AST), alanine transaminase (ALT), lactic dehydrogenase (LDH), and corticosterone levels. Also oxidative markers such as malondialdehyde (MDA) and tumor necrosis factor‐α (TNF‐α), and the antioxidative enzyme, catalase were measured. Adrenal glands were processed for light and transmission electron microscopic study. The results showed a significant increase in serum liver enzymes (AST, ALT, and LDH), corticosterone, MDA, and TNF‐α levels and a significant decrease in serum levels of catalase in IR‐group compared with SC‐group. Adrenal cortical tissue of IR‐group showed the loss of normal appearance. Some cells of zona glomerulosa and most of the zona fasciculata cells appeared swollen and degenerated with highly vacuolated cytoplasm. Other cells were shrunken with deeply acidophilic cytoplasm and pyknotic nuclei. Degenerated mitochondria with disrupted cristae, lipid droplets were confluent and dilated smooth endoplasmic reticulum were seen. Few zona reticularis cells had the dark nucleus and cytoplasmic vacuolations. In the different zones, blood capillaries were markedly congested and some inflammatory cells infiltrations were observed. Liver IR affected the structure of the adrenal cortex.

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Section: Discussionmentioning

confidence: 99%

The possible structural changes in the adrenal gland cortex after induction of hepatic ischemia–reperfusion injury in male albino rats: Light and electron microscopic study

El‐Tahawy

Abozaid

2019

Journal Cellular Physiology

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“…The adrenal gland is the most susceptible of the endocrine tissues to compound-induced lesions, with the zona fasciculata and reticularis being the most frequently affected zones (Gopinath, Prentice, and Lewis 1987). Several compounds such as alpha-(1,4-dioxide-3-methylquinoxalin-2-yl)-N-methylnitrone; oxymetholone; 2,3 0 ,4,4 0 ,5-pentachlorobiphenyl and 2,3,7,8-tetrachlorodibenzo-p-dioxin cause widespread vacuolization of adrenal cortical cells in rats and dogs (Yarrington et al 1985;Gopinath, Prentice, and Lewis 1987;NTP 1999NTP , 2006bNTP , 2010b. Increased adrenal cortical cytoplasmic vacuolation has been reported in 5 of the 8 studies designed specifically to evaluate the toxic equivalency factors for polyhalogenated aromatic hydrocarbons in female SD rats (NTP Technical Reports 520,521,525,526,529,530,531,and 559).…”

Section: Discussionmentioning

confidence: 99%

Distinguishing Cystic Degeneration from Other Aging Lesions in the Adrenal Cortex of Sprague-Dawley Rats

Laast¹,

Larsen

Allison

et al. 2014

Toxicol Pathol

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Cystic degeneration of the adrenal cortex is a common age-related finding in the Sprague-Dawley (SD) rat strain occurring more frequently in females. Compression of the adjacent cortex, a common hallmark of benign adrenal cortical tumors, often accompanies foci of cystic degeneration, creating a diagnostic challenge. Accurately differentiating these relatively common degenerative changes from proliferative lesions is critical in safety assessment studies. Cystic degeneration typically arises in the zona fasciculata of the adrenal cortex and often causes compression along the margin of the lesion. The degenerating cells are large, with abundant eosinophilic cytoplasm, or contain clear cytoplasmic vacuoles. Mitotic figures are generally uncommon. In many cases, cystic degeneration appears to arise in areas of hypertrophy in the zona fasciculata. In contrast, adrenal cortical hyperplasia and adrenal cortical adenoma are frequently comprised of smaller cells that cause compression of adjacent cortex, and in some cases mitotic figures are observed. Cytological detail and growth patterns should be considered more useful criteria than compression alone for separating degenerative cystic lesions from proliferative lesions in the adrenal cortex of SD rats.

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“…DMNM ( -[1,4-dioxido-3-methylquinoxalin-2-yl]-N-methylnitrone) is an antibiotic that causes impaired steroidogenesis, likely by blocking the conversion of cholesterol to pregnenolone. After acute exposure, it results in cytoplasmic vacuolation of the zona fasciculata and reticularis (26,28). Chemicals that induce severe vacuolar degeneration, like DMNM, often lead to loss of adrenocortical cells due to necrosis, cell lysis, or apoptosis.…”

Section: Manifestations Of Toxicity Of the Adrenal Cortexmentioning

confidence: 99%

Adrenal Gland: Structure, Function, and Mechanisms of Toxicity

et al. 2001

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The adrenal gland is one of the most comm on endocrine organs affected by chemically induced lesions. In the adrenal cortex, lesions are more frequent in the zona fasciculata and reticularis than in the zona glomerulosa. The adrenal cortex produces steroid hormones with a 17-carbon nucleus following a series of hydroxyla tion reactions that occur in the m itochondria and endoplasm ic reticulum. Toxic agents for the adrenal cortex include short-chain aliphatic compound s, lipidosis inducers , amphiphilic compounds , natural and synthetic steroids, and chemicals that affect hydroxyla tion. Morphologic evaluation of cortical lesions provides insight into the sites of inhibition of steroidogenesis. The adrenal cortex response to injury is varied. Degeneratio n (vacuolar and granular), necrosis, and hem orrhage are common ndings of acute injury. In contrast, chronic reparative processes are typically atrophy, brosis, and nodular hyperplasia. Chem ically induced proliferative lesions are uncom m on in the adrena l cortex. The adrenal medulla contains chrom af n cells (that produce epinephrine, norepineph rine, chromogranin, and neuropeptides) and ganglion cells. Proliferative lesions of the medulla are common in the rat and include diffuse or nodular hyperplasia and benign and malignant pheochrom ocytoma. Mechanism s of chromaf n cell proliferation in rats include excess growth hormone or prolactin, stimulation of cholinergic nerves, and diet-induced hypercalcem ia. There often are species speci city and age dependenc e in the developme nt of chemically induced adrenal lesions that should be considered when interpreting toxicity data.

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Degeneration of the rat and canine adrenal cortex caused by ?-(1,4-dioxido-3-methylquinoxalin-2-yl)-N-methylnitrone (DMNM)

Cited by 13 publications

References 10 publications

The possible structural changes in the adrenal gland cortex after induction of hepatic ischemia–reperfusion injury in male albino rats: Light and electron microscopic study

The possible structural changes in the adrenal gland cortex after induction of hepatic ischemia–reperfusion injury in male albino rats: Light and electron microscopic study

Distinguishing Cystic Degeneration from Other Aging Lesions in the Adrenal Cortex of Sprague-Dawley Rats

Adrenal Gland: Structure, Function, and Mechanisms of Toxicity

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