Citrate Uptake and Oxidation by Fragments of
Rat Ventral Prostate

Rb, Franklin; Costello, Leslie C.

doi:10.1159/000458507

Cited by 22 publications

(18 citation statements)

References 5 publications

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“…These studies along with our previous re ports (3,4) continue to emphasize that limited citrate oxidation is a significant factor in prostate citrate accumulation and secretion. At present the conversion of citrate to isocitrate appears to be a key reaction in this limitation.…”

Section: Resultssupporting

confidence: 53%

“…Earlier reports from this laboratory (3,4) have reviewed the possible relationship of decreased citrate oxidation as a possible key factor in prostate metabolism. With the use of teased fragments of ventral prostate lobes, Franklin et al (4) reported a very limited citrate oxidation that might ac count for prostatic citrate accumulation. With isolated mitochondrial preparations, Costello et al (3) demonstrated the existence of IDH activity but little citrate stimulation of IDH activity.…”

mentioning

confidence: 99%

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Citrate and Isocitrate Utilization by Rat Ventral Prostate Mitochondria

Costello¹,

Fadika²,

Franklin³

1978

Enzyme

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Isolated rat ventral prostate mitochondria preparations were capable of utilizing exogenous isocitrate with some resulting production of citrate. The prostate preparation did not utilize citrate or aKG. Citrate utilization via isocitrate seems to be limited by a unique aconitase activity which permits isocitrate to citrate but not citrate to isocitrate conversion. In contrast, kidney cortex mitochondria (under these same conditions) were capable of utilizing citrate, isocitrate, and aKG, and also converting isocitrate to citrate. The results support the view that citrate oxidation by prostate may be limited at the aconitase step, and thus may be a key step in accounting for the uniquely high citrate content of prostate.

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Section: Resultssupporting

confidence: 53%

mentioning

confidence: 99%

Citrate and Isocitrate Utilization by Rat Ventral Prostate Mitochondria

Costello¹,

Fadika²,

Franklin³

1978

Enzyme

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“…If maconitase activity is functionally limiting, the citrate/isocitrate ratio will increase significantly, provided that citrate synthesis occurs. This is precisely the condition that occurs with citrate-producing prostate epithelial cells [23,24]. The inhibition of m-aconitase activity by zinc results in a cellular citrate/ isocitrate ratio ~30/1.…”

Section: (A)mentioning

confidence: 91%

‘Why do tumour cells glycolyse?’: From glycolysis through citrate to lipogenesis

2005

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The re-emergence of interest in intermediary metabolism and the development of metabolomics in relation to cancer and other diseases provide a timely reason to revisit issues of tumour cell metabolism. In this review, we address the issue of the role of high aerobic glycolysis, which is commonly associated with the metabolism of many tumour cells. The concept presented emphasises the importance of the glycolysis-citrate-lipogenesis pathway in providing the synthetic and bioenergetic requirements that are essential for the growth and proliferation of tumour cells. We hope that our discussion will be informative and instructive, and will stimulate interest and research regarding the intermediary metabolism and its regulation in tumour cells. We express our appreciation to the many pioneering and contemporary researchers whose studies provide much of the basis for this presentation.

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“…Pursuant studies by Costello et al (1976) demonstrated that prostate mitochondria exhibited a low m-aconitase activity that limited citrate oxidation. Further evidence for a limiting maconitase activity in prostate cells is obtained from the uniquely high citrate/isocitrate ratio ~30-40/1 (Costello et al, 1978;Franklin et al, 1977). Recent studies demonstrated that normal citrate-producing prostate cells contain typical levels of m-aconitase enzyme Liu et al, 1996) Therefore m-aconitase activity must be limited by (1) unique properties of prostate m-aconitase which limit the conversion of citrate to isocitrate, and/or (2) unique intramitochondrial conditions which inhibit the m-aconitase reaction.…”

Section: M-aconitase and Net Citrate Productionmentioning

confidence: 99%

Mitochondrial function, zinc, and intermediary metabolism relationships in normal prostate and prostate cancer

2005

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Human prostate secretory epithelial cells have the uniquely specialized function of accumulating and secreting extremely high levels of citrate. This is achieved by their ability to accumulate high cellular levels of zinc that inhibit citrate oxidation. This process of net citrate production requires unique metabolic/bioenergetic mitochondrial relationships. In prostate cancer, the malignant cells undergo a metabolic transformation from zinc-accumulating citrate-producing sane cells to citrateoxidizing malignant cells that lost the ability to accumulate zinc. This review describes the metabolic/bioenergetic, zinc and mitochondrial relationships involved in normal and malignant prostate. Hopefully, this report will generate much needed interest and research in this neglected, but critically important, area of investigation.

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Citrate Uptake and Oxidation by Fragments of Rat Ventral Prostate

Cited by 22 publications

References 5 publications

Citrate and Isocitrate Utilization by Rat Ventral Prostate Mitochondria

Citrate and Isocitrate Utilization by Rat Ventral Prostate Mitochondria

‘Why do tumour cells glycolyse?’: From glycolysis through citrate to lipogenesis

Mitochondrial function, zinc, and intermediary metabolism relationships in normal prostate and prostate cancer

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