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Journal ArticleDOI

Does excessive adenosine 5′-triphosphate formation in cells lead to malignancy? A hypothesis on cancer

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TLDR
This work has suggested that mitochondrial complex I and the glycolytic enzyme glyceraldehyde 3-phosphate dehydrogenase (GA3PD) may be critically altered specifically in malignant cells and it is proposed that this excessive ATP formation may be due to altered mitochondrialcomplex I and GA3PD ofmalignant cells.
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This article is published in Medical Hypotheses.The article was published on 1997-06-01. It has received 13 citations till now. The article focuses on the topics: ATP hydrolysis & Adenosine triphosphate.

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Journal ArticleDOI

Cellular distribution and functions of P2 receptor subtypes in different systems.

TL;DR: This review is aimed at providing readers with a comprehensive reference article about the distribution and function of P2 receptors in all the organs, tissues, and cells in the body.
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Mitochondria and energetic depression in cell pathophysiology.

TL;DR: A metabolic shift characterized by suppression of OXPHOS combined with activation of aerobic glycolysis as the main pathway for ATP synthesis (Warburg effect) is of central importance to avoid CED and to control the cellular redox state, thereby ensuring the cell survival.
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Critical evaluation of toxic versus beneficial effects of methylglyoxal.

TL;DR: The potential beneficial effects of methylglyoxal far outweigh its possible toxic role in vivo, and it should be utilized for the benefit of suffering humanity.
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Atrophic gastritis: deficient complex I of the respiratory chain in the mitochondria of corpus mucosal cells

TL;DR: Corpus dominant atrophic gastritis is characterized by decreased respiratory capacity and relative deficiency of the respiratory complex I of mitochondria in the mucosa, the latter defect probably limiting mitochondrial ATP production and energetic support of the secretory function of the zymogenic mucosal cells.
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Cancer morphogenesis: role of mitochondrial failure.

TL;DR: The role of mitochondrial dysfunction in cancer morphogenesis is clarified and it is elucidated how faulty morphogen gradient signaling and inflammatory mediators that regulate OXPHOS can cause cancer-induced morphogenesis.
References
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Book

Principles of Biochemistry

TL;DR: The third edition, coming ten years after the first, emphasizes both the flowering of biochemical research and the prodigious effort by busy teachers and scientists to keep up to date this popular text and reference.
Book

Molecular Biology of the Gene

TL;DR: The long-awaited Fifth Edition of James D. Watson's classic text, Molecular Biology of the Gene, has been thoroughly revised and is published to coincide with the 50th anniversary of Watson and Crick's paper on the structure of the DNA double-helix as discussed by the authors.
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Biochemistry (4th edn)

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Inhibition of electron flow through complex I of the mitochondrial respiratory chain of Ehrlich ascites carcinoma cells by methylglyoxal

TL;DR: The results indicate that methylglyoxal strongly inhibits ADP-stimulated alpha-oxo-glutarate and malate plus pyruvate-dependent respiration, whereas, at a much higher concentration, methyl glyoxal fails to inhibit succinate- dependent respiration.
Journal ArticleDOI

Inhibition of glycolysis and mitochondrial respiration of Ehrlich ascites carcinoma cells by methylglyoxal.

TL;DR: Study reported herein strongly suggest that the tumoricidal effect of MG is mediated at least in part through the inhibition of mitochondrial respiration and inactivation of GA3PD, and this enzyme may play an important role in the high glycolytic capacity of the malignant cells.
Related Papers (5)
Trending Questions (1)
What happens in the case of excess ATP in the cell?

Excessive ATP formation in a cell may lead to uncontrolled cell growth and malignancy.