Hepatic Kupffer cell function: the efficiency of uptake and intracellular degradation of 14C-labelled mitochondria is reduced in aged rats

Martin, Glenn E; Sewell, R. B.; Yeomans, Neville D; Morgan, Denis J.; Smallwood, Richard A.

doi:10.1016/0047-6374(94)90048-5

Cited by 9 publications

(9 citation statements)

References 22 publications

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“…The large lysosomal component (13.5% of the cell volume) of the Kupffer cell, together with its high specific activity of lysosomal enzymes, suggests a considerable capacity to degrade ingested substances. [16] The liver also contains a large resident and migratory population of lymphocytes [Figure 8] that provide immune surveillance against foreign antigens. This population can be rapidly increased in response to infection or injury by hiring leucocytes from the circulation.…”

Section: Discussionmentioning

confidence: 99%

Histological changes in the liver of fetuses of pregnant rats following citalopram administration

et al. 2013

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Objective:Depression is a dilapidating disorder, which may occur during pregnancy. Citalopram is an antidepressant drug often prescribed to pregnant women. The purpose of the present study is to determine whether maternal administration of citalopram affects fetal liver histology.Materials and Methods:Pregnant Wistar albino rats were treated with citalopram (10 or 20 mg/kg/day). A control group received no treatment. Rat fetal liver samples were obtained on day 18 of gestation and evaluated morphologically and histologically.Results:Statistical evaluation of data showed that there were no differences in liver weight and relative liver weight between control and citalopram treatment groups. Liver histology changes (such as increases in the number of Kupffer cells and lymphocytes) were seen in the fetuses of the group receiving a high dose of citalopram during gestation. Degeneration of hepatocytes was not seen and the megakaryocyte number did not change significantly in the citalopram treated groups.Conclusion:This study showed that citalopram administration during gestation may have some adverse effects on the phagocytic cell population in the fetal liver of rats.

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Section: Discussionmentioning

confidence: 99%

Histological changes in the liver of fetuses of pregnant rats following citalopram administration

et al. 2013

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“…) and efficiency to phagocytose and degrade radiolabelled mitochondria (Martin et al . ). This perhaps leads to more severely damaged mitochondria that accumulate with age.…”

Section: Energy Metabolism In Brain Ageing and Alzheimer's Diseasementioning

confidence: 97%

Mitochondrial function in ageing: coordination with signalling and transcriptional pathways

Yin

Sancheti

Liu

et al. 2015

The Journal of Physiology

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Mitochondrial dysfunction entailing decreased energy-transducing capacity and perturbed redox homeostasis is an early and sometimes initiating event in ageing and age-related disorders involving tissues with high metabolic rate such as brain, liver and heart. In the central nervous system (CNS), recent findings from our and other groups suggest that the mitochondrion-centred hypometabolism is a key feature of ageing brains and Alzheimer's disease. This hypometabolic state is manifested by lowered neuronal glucose uptake, metabolic shift in the astrocytes, and alternations in mitochondrial tricarboxylic acid cycle function. Similarly, in liver and adipose tissue, mitochondrial capacity around glucose and fatty acid metabolism and thermogenesis is found to decline with age and is implicated in age-related metabolic disorders such as obesity and type 2 diabetes mellitus. These mitochondrion-related disorders in peripheral tissues can impact on brain functions through metabolic, hormonal and inflammatory signals. At the cellular level, studies in CNS and non-CNS tissues support the notion that instead of being viewed as autonomous organelles, mitochondria are part of a dynamic network with close interactions with other cellular components through energy-or redox-sensitive cytosolic kinase signalling and transcriptional pathways. Hence, it would be critical to further understand the molecular mechanisms involved in the communication between mitochondria and the rest of the cell. Therapeutic strategies that effectively preserves or improve mitochondrial function by targeting key component of these signalling cascades could represent a novel direction for numerous mitochondrion-implicated, age-related disorders.

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“…It appears that in rat liver Kupffer cell function declines with age, but endocytosis by endothelial cells remains unchanged [22,23]. The implications of those changes in humans are unknown because studies of the macrophage function of Kupffer cells with aging are rare.…”

Section: Reticuloendothelial System Functionmentioning

confidence: 99%

“…This suggests that the size of the Kupffer cell population does not increase with age. Furthermore, the capacity of Kupffer cells to phagocytize and degrade radiolabeled mitochondria is less efficient [23]. Their role in the production or degradation of cytokines has not been studied during aging.…”

Section: Reticuloendothelial System Functionmentioning

confidence: 99%

“…The implications of those changes in humans are unknown because studies of the macrophage function of Kupffer cells with aging are rare. In one study performed in rats [23], there was no change in the volume density of Kupffer cells between 2 and 24 months of age. This suggests that the size of the Kupffer cell population does not increase with age.…”

Section: Reticuloendothelial System Functionmentioning

confidence: 99%

See 1 more Smart Citation

Aging Liver

Anantharaju¹,

Feller²,

Chedid³

2002

Gerontology

166

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Aging is characterized by a progressive decline of cellular functions. The aging liver appears to preserve its function relatively well. Aging is associated in human liver with morphological changes such as decrease in size attributable to decreased hepatic blood flow. Ultrastructural analysis of the human liver has revealed that the integrity of mitochondria and enzymatic activity remain mostly unchanged with aging. Reactive oxygen species (ROS) are involved in the aging process and result mainly from nonenzymatic processes in the liver. Endogenous free radicals are generated within mitochondria and suspected to cause severe injury to mitochondrial DNA. This damaged DNA accumulates with aging. In addition, polyunsaturated fatty acids, highly sensitive to ROS, decrease in liver mitochondria from human centenarians, a feature acquired during evolution as a protective mechanism to favor longevity. Diet is considered the main environmental factor having effect on lifespan. It has a major impact on aging liver, the central metabolic organ of the body. The ubiquitin proteolytic pathway in the liver serves to destroy many proteins, among them p21 which is encoded by abundant mRNA in senescent cells, can inhibit cell proliferation and favors DNA repair. Drug therapy in the elderly may be complicated by several factors such as decline in body weight, renal function, liver mass and hepatic blood flow, making adverse drug reactions more frequent. Hepatic drug metabolism is mainly mediated by the cytochrome P₄₅₀system and drug interactions in the elderly are likely related to the progressive decline of this system after the fifth decade of life and another decrease in individuals aged >70. Antihypertensive therapy in the elderly depends upon either hepatic or renal function and should be adjusted accordingly. Finally, telomerases are the biological clocks of replicative lifespan. Shortening of telomeric ends of chromosomes correlates with aging and decline in the replicative potential of the cell: replicative senescence. Telomere DNA of human somatic cells shortens during each cell division thus leading to a finite proliferation. Transfection of the telomerase reverse transcriptase gene results in elongation of telomeres and extension of lifespan. This also applies to humans. Replicative senescence in human cells evolved as a mechanism to protect them from continuous divisions leading to multiple mutations. Longer-lived species such as humans had to develop replicative senescence to ensure that they would have the increased protection that their longevity necessitates.

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Hepatic Kupffer cell function: the efficiency of uptake and intracellular degradation of 14C-labelled mitochondria is reduced in aged rats

Cited by 9 publications

References 22 publications

Histological changes in the liver of fetuses of pregnant rats following citalopram administration

Histological changes in the liver of fetuses of pregnant rats following citalopram administration

Mitochondrial function in ageing: coordination with signalling and transcriptional pathways

Aging Liver

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