Oxidative activity in mitochondria isolated from rat liver at different stages of development

Iossa, Susanna; Lionetti, Lillà; Mollica, Maria Pina; Barletta, Antonio; Liverini, Giovanna

doi:10.1002/(sici)1099-0844(1998120)16:4<261::aid-cbf796>3.0.co;2-1

Cited by 5 publications

(4 citation statements)

References 30 publications

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“…Maximal oxygen consumption rates were measured in homogenates and isolated mitochondria polarographically with a Clark-type electrode (Yellow Springs Instruments, Yellow Springs, Ohio), maintained in a water-jacketed chamber at 30°C, as previously reported [16]. Briefly, aliquots of homogenates and isolated mitochondria were incubated in 3 ml of the above suspension medium and were allowed to oxidise their endogenous substrates for a few minutes.…”

Section: Measurement Of Respiration In Liver Homogenates and Mitochonsupporting

confidence: 58%

Acetyl-L-carnitine treatment stimulates oxygen consumption and biosynthetic function in perfused liver of young and old rats

Mollica

Iossa

Soboll

et al. 2001

CMLS, Cell. Mol. Life Sci.

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The effect of treatment with acetyl-L-carnitine on hepatic mitochondrial respiration and biosynthetic function in perfused liver from young (90 days) and old (22-24 months) rats was studied. Rats were given a 1.5% (w/v) solution of acetyl-L-carnitine in their drinking water for 1 month and oxygen consumption together with the rate of gluconeogenesis, urea synthesis, and ketogenesis with and without added substrates were measured in perfused liver. Mitochondrial oxygen consumption was also assessed in liver homogenate and isolated mitochondria to determine the maximal capacity for oxidative phosphorylation. Acetyl-L-carnitine treatment almost completely restored the age-dependent decline in oxygen consumption, gluconeogenesis, urea synthesis, and ketogenesis found in perfused liver of old rats to the levels found in young rats. In addition, acetyl-L-carnitine treatment increased oxygen consumption and biosynthetic function in perfused liver from young rats. After acetyl-L-carnitine treatment, we found detectable 3-oxoacyl-CoA-transferase activity associated with a consumption of ketone bodies in young and old rats. Finally, oxygen consumption measured in homogenate and isolated mitochondria did not change with age and acetyl-L-carnitine treatment. Our results show that in perfused liver, acetyl-L-carnitine treatment slows the age-associated decline in mitochondrial respiration and biosynthetic function. In addition, treatment of young rats with acetyl-L-carnitine has a stimulating effect on liver metabolism, probably through an increase in ATP production.

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Section: Measurement Of Respiration In Liver Homogenates and Mitochonsupporting

confidence: 58%

Acetyl-L-carnitine treatment stimulates oxygen consumption and biosynthetic function in perfused liver of young and old rats

Mollica

Iossa

Soboll

et al. 2001

CMLS, Cell. Mol. Life Sci.

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“…We have previously found that a decrease in FAD-linked respiration is the first age-linked biochemical impairment of energy-transducing pathways which could be detected in liver mitochondria from 180-day-old rats [3,4]. This finding is in line with other results in which tissue ageing is associated with a decrease in electron transport chain enzyme activity [5].…”

Section: Cmls Cellular and Molecular Life Sciencessupporting

confidence: 81%

“…In this work, we found that the decline in succinate-supported state 3 respiration previously observed in adult rats [3,4] is due to a decrease in COX activity and ANT content. COX activity and ANT are known to exert a strong control over liver respiration [27,28].…”

Section: Discussionmentioning

confidence: 99%

“…In fact, a postulated role for incomplete mitochondrial coupling is protection against ROS [6], whose production increases when oxygen consumption rates are low and the degree of reduction of the components of the electron transport chain is high. Taking into account that in 180-day-old rats we found a decrease in oxidative rates and COX activity without any change in succinic dehydrogenase activity as previously shown [3], in adult rats, increased palmitateinduced leak possibly functions to avoid excess ROS damage. Consistent with this role, we found that in 180-day-old rats, compared to 60-day-old ones, there is no variation in the specific activity of superoxide-sensitive mitochondrial enzyme aconitase.…”

Section: Discussionmentioning

confidence: 99%

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Modulation of hepatic mitochondrial energy efficiency with age

Lionetti

Crescenzo

Mollica

et al. 2004

Cellular and Molecular Life Sciences (CMLS)

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This study was designed to examine the effect of youth-adulthood transition on hepatic mitochondrial energy efficiency. The changes in basal and palmitate-induced proton leak, which contribute to mitochondrial efficiency, were evaluated in mitochondria isolated from the liver of young and adult rats. Alterations in mitochondrial cytochrome oxidase and aconitase specific activities, and in adenine nucleotide translocator content were also assessed. There was no difference in basal proton leak or thermodynamic coupling and efficiency of oxidative phosphorylation in liver mitochondria between the two rat groups. On the other hand, palmitate-induced proton leak increased significantly in adult rats. The function of this uncoupling could be avoidance of elevated formation of reactive oxygen species, which are known to accelerate ageing.

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Diabetes and mitochondrial bioenergetics: Alterations with age

Ferreira

Palmeira

Seiça

et al. 2003

J Biochem & Molecular Tox

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Several studies have been carried out to evaluate the alterations in mitochondrial functions of diabetic rats. However, some of the results reported are controversial, since experimental conditions, such as aging, and/or strain of animals used were different. The purpose of this study was to evaluate the metabolic changes in liver mitochondria, both in the presence of severe hyperglycaemia (STZ-treated rats) and mild hyperglycaemia (Goto-Kakizaki (GK) rats). Moreover, metabolic alterations were evaluated both at initial and at advanced states of the disease. We observed that both models of type 1 and type 2 diabetes presented alterations on respiratory chain activity. Because of continual severe hyperglycaemia, 9 weeks after the induction of diabetes, the respiratory function declined in STZ-treated rats, as observed by membrane potential and respiratory ratios (RCR, P/O, and FCCP-stimulated respiration) assessment. In contrast, GK rats of 6 months age presented increased respiratory ratios. To localize which respiratory complexes are affected by diabetes, enzymatic respiratory chain activities were evaluated. We observed that succinate dehydrogenase and cytochrome c oxidase activities were significantly augmented both in STZ-treated rats and GK rats of 6 months age. Moreover, H(+)-ATPase activity was also significantly increased in STZ-treated rats with 3 weeks of diabetes and in GK rats of 6 months age as compared to controls. Therefore, these results clearly suggest that both animal models of diabetes present some metabolic adjustments in order to circumvent the deleterious effects promoted by the high glucose levels typical of the disease.

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Oxidative activity in mitochondria isolated from rat liver at different stages of development

Cited by 5 publications

References 30 publications

Acetyl-L-carnitine treatment stimulates oxygen consumption and biosynthetic function in perfused liver of young and old rats

Acetyl-L-carnitine treatment stimulates oxygen consumption and biosynthetic function in perfused liver of young and old rats

Modulation of hepatic mitochondrial energy efficiency with age

Diabetes and mitochondrial bioenergetics: Alterations with age

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