The aging of rat liver as revealed by electron microscopic morphometry—I. Basic parameters

Pieri, Carlo; Zs-Nagy, I; Mazzufferi, G; Giuli, C.

doi:10.1016/0531-5565(75)90006-6

Cited by 63 publications

(38 citation statements)

References 21 publications

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“…DePriester et al (22) suggested that an age-associated increase in the hepatocyte binuclear B315 B316 SCHMUCKER index, coupled with no change in hepatocyte volume, results in an increase in the nucleocytoplasmic ratio. In agreement with this and other studies, our own analyses demonstrated that age-associated changes in the hepatocyte nucleocytoplasmic ratio reflected concomitant shifts in cell and nuclear volumes (21,23,24; see Figure 1). Although aging appears to be accompanied by an increase in hepatocyte nuclear ploidy, changes in cell and/or nuclear volumes are less apparent owing, in part, to an age-associated increase in interindividual variability.…”

Section: Liver Morphologysupporting

confidence: 76%

“…This observation correlates well with a concomitant decline in the yield of liver microsomal protein from similarly aged rats of the same strain (42). The only other study to measure SER surface area in rat hepatocytes during aging reported an initial loss of membrane followed by an increase during maturation and senescence, such that the oldest animals examined contained similar or greater amounts of this organelle than young rats (24). The fact that the liver contains a heterogenous population of hepatocytes (a) whose individual ages do not correlate directly with host age and (b) that exhibit structural differences according to their sublobular location may obscure age-associated changes in cell structure.…”

Section: Liver Morphologymentioning

confidence: 50%

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Aging and the Liver: An Update

Schmucker

1998

The Journals of Gerontology Series A: Biological Sciences and M

164

104

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Section: Liver Morphologysupporting

confidence: 76%

Section: Liver Morphologymentioning

confidence: 50%

Aging and the Liver: An Update

Schmucker

1998

The Journals of Gerontology Series A: Biological Sciences and M

164

104

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“…1,2,23 These results are consistent with past studies, all of which conclude that there are few gross structural changes in the liver with age. 1,2,23 Previous electron-microscopic studies have not reported specific investigations of sinusoidal structures in the intact aged liver 14,[24][25][26][27] ; however, our assessment by electron microscopy and immunohistochemistry revealed significant age-related changes within the sinusoidal endothelium and space of Disse. Scanning electron microscopy revealed a significant reduction in the porosity of the aged sinusoidal endothelium.…”

Section: Discussioncontrasting

confidence: 45%

Pseudocapillarization and associated energy limitation in the aged rat liver

2001

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Age-related impairment of drug metabolism by the liver is consistent with hepatocyte hypoxia, suggestive of the development of a diffusional barrier to oxygen supply. Because the effects of aging on the diffusional pathway (sinusoidal endothelium and space of Disse) have not been described, we performed comparative studies on the livers of Fischer F344 rats aged 4 to 7, 12 to 15, and 24 to 27 months. Lightmicroscopic examination revealed no evidence of fibrosis, cirrhosis, or other specific pathology. In contrast, scanning and transmission electron-microscopic examination revealed that aging is associated with pseudocapillarization of the sinusoidal endothelium, indicated by defenestration with reduced porosity, thickening of the endothelium, infrequent development of basal lamina, and only minor collagen deposits in the space of Disse. Furthermore, immunohistochemistry studies showed strong expression of collagen IV, moderate expression of factor VIII-related antigen, and weak expression of collagen I along the sinusoids of livers from old rats (P < .0001). In vitro 31 P magnetic resonance spectroscopy analysis showed that aging is associated with changes in high-energy phosphate and other metabolites, consistent with hepatocyte hypoxia. Aging in the liver is associated with changes in the sinusoidal endothelium and space of Disse that may restrict the availability of oxygen and other substrates. (HEPATOLOGY 2001;33:537-543.)The effect of aging in the liver is often considered to be of a lesser degree than in other organs. [1][2][3][4] The major recognized changes in the aging liver include reduction in liver mass and hepatic blood flow 1,4,5 ; however, it has been concluded that there are few other significant structural or biochemical changes in the liver. 1,2 On the other hand, even subtle agerelated changes may have profound consequences for the rest of the body. For example, any age-related impairment in hepatic drug and xenobiotic detoxification could partly explain the susceptibility of elderly persons to adverse drug reactions or illnesses with toxic etiology. 5 In vivo, the hepatic clearance of many drugs is reduced in elderly persons. Traditional theories have attempted to attribute this to age-related reduction of liver mass and blood flow. 6 However, in a recent review, 5 we noted that there appears to be selective reduction of the clearance of drugs that undergo phase I metabolism, associated with preservation of the clearance of drugs that undergo phase II metabolism. Even more puzzling, the in vitro activities of phase I enzymes are maintained into old age. 7 Because these paradoxes cannot be attributed to changes in blood flow and liver mass alone, we suggested an explanation based on oxygen supply, as the activities of phase I enzymes are highly oxygen-dependent because they require oxygen as a substrate. 8 We hypothesized the development of a barrier to oxygen diffusion, leading to functional intracellular hypoxia in the hepatocytes of the aging liver. This provides a plausible mechanism for i...

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“…Morphologic and biochemical cellular alterations have been observed in other aging organs [Mainwaring, 1968;Pieri et al, 1975;Brandes and Garcia-Buñuel, 1978], Such cellular changes in the aged uterus might have a significant adverse effect upon the ability of this organ, even when it is stimulated by exogenous ovarian hormones, to undergo decidualization.…”

Section: Discussionmentioning

confidence: 99%

Effect of Age upon Uterine Response to Deciduagenic Stimulus

Craig¹

1981

Cells Tissues Organs

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The effect of aging upon ability of the uterus to respond to a deciduagenic stimulus was studied by transmission electron microscopy. Particularly, subtle structural characteristics of decidualization were sought in stromal cells of uteri of aged rats. To negate effects of ovarian aging, rats 4, 10 and 20–24 months of age were subjected to bilateral ovariectomy and subsequent ovarian hormone injections. As deciduagenic stimulus, sesame oil was injected into the right uterus. The left served as the hormone primed control; and only antimesometrial endometrium was examined. Oil-injected uteri of 4- and 10-month-old rats developed deciduomata which histologically were similar to published descriptions. No decidual changes were observed in the aged oil-injected uterus. Therefore, the experimental and control uteri appeared similar. Luminal epithelial cells of aged rats differed from those of younger animals primarily in possessing more lysosomes and fewer surface microvilli. Stromal cells of aged rats differed more in shape and in quantity of cytoplasm, and in these cells lipofuscin deposits were identified more frequently. Moreover, leukocytes, plasma cells and macrophages were more numerous in the aged uteri. Failure of the aged uterus to decidualize could not be correlated with any morphologic changes. Results are correlated with previously proposed explanations for failure of aged uteri to decidualize and, accordingly, to maintain implanting embryos.

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The aging of rat liver as revealed by electron microscopic morphometry—I. Basic parameters

Cited by 63 publications

References 21 publications

Aging and the Liver: An Update

Aging and the Liver: An Update

Pseudocapillarization and associated energy limitation in the aged rat liver

Effect of Age upon Uterine Response to Deciduagenic Stimulus

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