Morphological and functional studies during aging at mitochondrial level. action of drugs

Cruz, Julia E. de la; Burón, Isabel; Roncero, Isabel

doi:10.1016/0020-711x(90)90008-q

Cited by 17 publications

(3 citation statements)

References 16 publications

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“…It has been showed that aging in rodents is associated with some decline of mitochondrial function with mitochondria from old mice characterized by less regular and more heterogeneous cristae not arranged in parallel stacks [18], and increased content of oxidation products of phospholipids, proteins and DNA, decreased membrane potential, and increased mitochondrial size and fragility [19]. It was revealed that aging in rodents [20][21][22] and humans [22] is associated with the increase in individual mitochondrial volume and decline in the number of mitochondria in the liver. These findings are supported by our observation of the increased matrix electron density of mitochondria in hepatocytes of old rats.…”

Section: Discussionmentioning

confidence: 99%

Short-term fenofibrate treatment improves ultrastructure of hepatocytes of old rats

Zubrzycki

Wrońska

Zauszkiewicz-Pawlak

et al. 2021

Folia Histochem Cytobiol.

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Introduction. Fenofibrate (FN) is a hypolipemic drug used for the treatment of mixed dyslipidemia. Since in our previous study FN administration to young and old rats adversely affected the serum activity of liver marker enzymes, we decided to examine the effects of FN on liver ultrastructure of young and old animals.Material and methods. Young and old rats were fed standard rodent chow supplemented with 0.1% FN for 30 days. Liver samples obtained from animals under full anesthesia were processed by routine methods to obtain ultrathin and histological sections for the examination by light microscopy (LM) and transmission electron microscopy (TEM). Furthermore, liver lysates were analyzed by Western blotting for the expression of the autophagy-related proteins LC3A/B and beclin 1.Results. The ultrastructure of hepatocytes in both age groups was well-preserved, with the presence of abundant mitochondria, numerous peroxisomes and lysosomes, glycogen stored in the form of rosettes, and occasionally autolysosomes. However, hepatocytes of old control rats contained less mitochondria and peroxisomes, and more lipid droplets than cells of young animals. The effects of FN on liver ultrastructure were age-depended. FN increased the relative number of mitochondria and peroxisomes in the hepatocytes of old, and did not affect their number in young rats. Moreover, FN decreased and increased the relative number of lipid droplets in the hepatocytes of old and young rats, respectively. At the LM level, Oil Red O staining revealed smaller and larger lipid droplets within hepatocytes and non-parenchymal liver cells. In the livers of young and old rats lipid droplets were distributed mainly in the periportal zones of hepatic lobules. Morphometric analysis confirmed that livers of control old rats contained more lipid-stainable areas than those of young ones; however, no effect of FN was observed either in young or old rats. Despite larger size of autolysosomes and autophagic vacuoles in hepatocytes of old rats, the expression of autophagy-related proteins did not differ in the livers of control and fenofibrate-treated young and old animals. Conclusions.The results of our study suggest that fenofibrate, apart from its hypolipemic action, may have beneficial effect on the energy metabolism in the liver of old individuals by increasing the number of mitochondria and peroxisomes in hepatocytes.

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Section: Discussionmentioning

confidence: 99%

Short-term fenofibrate treatment improves ultrastructure of hepatocytes of old rats

Zubrzycki

Wrońska

Zauszkiewicz-Pawlak

et al. 2021

Folia Histochem Cytobiol.

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“…For example, the Ca2+ binding proteins calmodulin and calbindin have been shown to decrease in quantity with age and in age-related diseases (Iacopino et al, 1990;Ichimiya et al, 1988;McLachlan et al, 1987;Teolato et al, 1983). Ca2+ accumulation in mitochondria also decreases with age, which may be related to exposure to reactive oxygen and mutation of mitochondrial DNA (dela Cruz et al, 1990;Hansford and Castro, 1982;Peterson et al, 1985;Richter, 1992;Schapira and Cooper, 1992). These changes in Ca2+ buffering would act to impair the expression of short-term forms of synaptic plasticity, like paired-pulse facilitation, that rely upon fine adjustments in the intracellular concentration of Ca2+.…”

Section: Discussionmentioning

confidence: 99%

Loss of paired‐pulse facilitation at the corticostriatal synapse of the aged rat

Walsh

1994

Synapse

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Changes in calcium (Ca2+) homeostasis have been proposed to contribute to the aging process. Paired-pulse facilitation, a form of synaptic enhancement that relies upon an accumulation of Ca2+ in the presynaptic terminal, was used to examine the effect of aging at the corticostriatal synapse. Intracellular recordings in striatal neurons from young rats demonstrated a consistent enhancement in the second of two synaptic responses evoked by stimulation of the corpus callosum. In contrast, neurons from aged rats showed a consistent depression of the second synaptic response at identical pairing intervals. These differences were not explained by an age-dependent increase in synaptic depression and demonstrate an alteration in the Ca(2+)-mediated process of presynaptic facilitation.

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“…Usually, mitochondrial size varies more in old cells, as compared to corresponding young cells, with a high proportion of large, sometimes extremely large "giant mitochondria" (14,60). Moreover, mitochondria undergo other structural modifications during aging such as loss or shortening of cristae, matrix vacuolization and inner membrane or cytoplasmic lamellae deterioration, which may be associated with agerelated impairment in mitochondrial membrane potential (14,61). Consequently, the number of defective mitochondria within long-lived postmitotic cells progressively increases with age.…”

Section: Age-related Neuronal Mitochondrial Dysfunctionmentioning

confidence: 99%

Protective action of green tea catechins in neuronal mitochondria during aging

Andrade¹

2015

Front Biosci

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Mitochondria are central players in the regulation of cell homeostasis. They are essential for energy production but at the same time, reactive oxygen species accumulate as byproducts of the electron transport chain causing mitochondrial damage. In the central nervous system, senescence and neurodegeneration occur as a consequence of mitochondrial oxidative insults and impaired electron transfer. The accumulation of several oxidation products in neurons during aging prompts the idea that consumption of antioxidant compounds may delay neurodegenerative processes. Tea, one of the most consumed beverages in the world, presents benefits to human health that have been associated to its abundance in polyphenols, mainly catechins, that possess powerful antioxidant properties in vivo and in vitro. In this review, the focus will be placed on the effects of green tea catechins in neuronal mitochondria. Although these compounds reach the brain in small quantities, there are several possible targets, signaling pathways and molecular machinery impinging in the mitochondria that will be highlighted. Accumulated evidence thus far seems to indicate that catechins help prevent neurodegeneration and delay brain function decline.

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Morphological and functional studies during aging at mitochondrial level. action of drugs

Cited by 17 publications

References 16 publications

Short-term fenofibrate treatment improves ultrastructure of hepatocytes of old rats

Short-term fenofibrate treatment improves ultrastructure of hepatocytes of old rats

Loss of paired‐pulse facilitation at the corticostriatal synapse of the aged rat

Protective action of green tea catechins in neuronal mitochondria during aging

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