Mitochondrial free radical generation, oxidative stress, and aging11This article is dedicated to the memory of our dear friend, colleague, and mentor Lars Ernster (1920–1998), in gratitude for all he gave to us.

Cadenas, Enrique; Davies, Kelvin J.A.

doi:10.1016/s0891-5849(00)00317-8

Cited by 2,552 publications

(700 citation statements)

References 53 publications

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“…(i) The uncoupling of mitochondria (low RCRs) can increase mitochondrial superoxide release (45), probably due to decreased heme availability (30,46). Decreased cytochrome concentration (18) of the electron-transport chain could also possibly contribute to increased superoxide levels.…”

Section: Further Mechanisms By Which Iron Deficiency Can Cause Damage Tomentioning

confidence: 99%

Iron deficiency and iron excess damage mitochondria and mitochondrial DNA in rats

Walter

Knutson

Paler-Martı́nez

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

304

182

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Approximately two billion people, mainly women and children, are iron deficient. Two studies examined the effects of iron deficiency and supplementation on rats. In study 1, mitochondrial functional parameters and mitochondrial DNA (mtDNA) damage were assayed in iron-deficient (<5 g͞day) and iron-normal (800 g͞day) rats and in both groups after daily high-iron supplementation (8,000 g͞day) for 34 days. This dose is equivalent to the daily dose commonly given to iron-deficient humans. Iron-deficient rats had lower liver mitochondrial respiratory control ratios and increased levels of oxidants in polymorphonuclear-leukocytes, as assayed by dichlorofluorescein (P < 0.05). Rhodamine 123 fluorescence of polymorphonuclear-leukocytes also increased (P < 0.05). Lowered respiratory control ratios were found in daily high-iron-supplemented rats regardless of the previous iron status (P < 0.05). mtDNA damage was observed in both iron-deficient rats and rats receiving daily high-iron supplementation, compared with ironnormal rats (P < 0.05). Study 2 compared iron-deficient rats given high doses of iron (8,000 g) either daily or every third day and found that rats given iron supplements every third day had less mtDNA damage on the second and third day after the last dose compared to daily high iron doses. Both inadequate and excessive iron (10 ؋ nutritional need) cause significant mitochondrial malfunction. Although excess iron has been known to cause oxidative damage, the observation of oxidant-induced damage to mitochondria from iron deficiency has been unrecognized previously. Untreated iron deficiency, as well as excessive-iron supplementation, are deleterious and emphasize the importance of maintaining optimal iron intake.

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Section: Further Mechanisms By Which Iron Deficiency Can Cause Damage Tomentioning

confidence: 99%

Iron deficiency and iron excess damage mitochondria and mitochondrial DNA in rats

Walter

Knutson

Paler-Martı́nez

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

304

182

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“…One of the mechanisms of male infertility is the excess production of reactive oxygen species (ROS) in sperm, which can induce nuclear DNA fragmentation, lipid peroxidation, and protein-protein cross links (2)(3)(4). The primary source of ROS in sperm is the respiratory chain of the mitochondrion (5)(6)(7)(8). The main ROS form in sperm is hydrogen peroxide (H 2 O 2 ), the concentration of which in sperm has not been measured (2)(3)(4), whereas in liver cells, the H 2 O 2 concentration (10 Ϫ7 to 10 Ϫ9 mol͞liter) is known to be 100-to 10,000-fold higher than that of superoxide (O 2 ⅐Ϫ ) (Ϸ10 Ϫ11 mol͞ liter) (6,9,10).…”

mentioning

confidence: 99%

Remarkably high activities of testicular cytochrome c in destroying reactive oxygen species and in triggering apoptosis

Liu

Lin

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Hydrogen peroxide (H2O2) is the major reactive oxygen species (ROS) produced in sperm. High concentrations of H 2O2 in sperm induce nuclear DNA fragmentation and lipid peroxidation and result in cell death. The respiratory chain of the mitochondrion is one of the most productive ROS generating systems in sperm, and thus the destruction of ROS in mitochondria is critical for the cell. It was recently reported that H 2O2 generated by the respiratory chain of the mitochondrion can be efficiently destroyed by the cytochrome c-mediated electron-leak pathway where the electron of ferrocytochrome c migrates directly to H 2O2 instead of to cytochrome c oxidase. In our studies, we found that mouse testisspecific cytochrome c (T-Cc) can catalyze the reduction of H 2O2 three times faster than its counterpart in somatic cells (S-Cc) and that the T-Cc heme has the greater resistance to being degraded by H 2O2. Together, these findings strongly imply that T-Cc can protect sperm from the damages caused by H 2O2. Moreover, the apoptotic activity of T-Cc is three to five times greater than that of S-Cc in a well established apoptosis measurement system using Xenopus egg extract. The dramatically stronger apoptotic activity of T-Cc might be important for the suicide of male germ cells, considered a physiological mechanism that regulates the number of sperm produced and eliminates those with damaged DNA. Thus, it is very likely that T-Cc has evolved to guarantee the biological integrity of sperm produced in mammalian testis. mouse testis ͉ antioxidation

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“…Oxidative stress has been implicated in the pathogenesis of many human diseases, the use of antioxidants in pharmacology is therefore much studied to treat especially stroke and neurodegenerative diseases (Ahmed and Tollefsbol, 2001;Anisimov, 2001;Artandi, 2006;Austad, 1993;Beckman and Ames, 1998;Besedovsky and Del, 2008;Blackburn, 2000;Cadenas and Davies, 2000;Campisi, 1997;Cong et al, 1999;Daynes and Araneo, 1992;Dirks and Leeuwenburgh, 2006;Fabris, 1991;Finkel and Holbrook, 2000;Franceschi, 1989;Hayflick, 2004;Holliday, 2006;Huerre and Gounon, 1996;Kanungo, 1975;Wick et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

One Can Slow Down the Aging through Antioxidants

Aversa¹,

Petrescu²,

Apicella³

et al. 2016

American Journal of Engineering and Applied Sciences

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Free radicals are natural nanoparticles which are doing their part well defined in the human cell, but then they must be annihilated or eliminated to not destroy the cell or another part of our body. It has been shown that residual free radicals in the body are responsible for the aging. The role to annihilate them is ful-filled by the antioxidants. Antioxidants are a group of compounds produced by the organism or that occur naturally in many foods. Antioxidants work together in the human body to maintain health and vigor, especially during the last decades of life. They do this by protecting us from harm caused by free radicals that can destroy skin and tissues healthy cells of the organism. Antioxidants are chemical compounds with many and varied applications. Naturally present in our diet, through fruits, vegetables, tea or red wine, they are recognized to be good for health. In fact, antioxidants protect our body's proteins and nucleic acids from oxidation. In the industry, antioxidants are also used as food additives to increase the shelf life of food. They are also present in the packaging or the wheels of cars because they prevent synthetic materials from becoming crumbly and brittle. Finally, in the cosmetics industry, creams containing antioxidants are known for their anti-aging properties. An antioxidant is a molecule that decreases or prevents the oxidation of other chemicals. Oxidation is part of an oxidation-reduction reaction that transfers electrons from a substance to an oxidizing agent. This reaction can produce radicals that cause destructive chain reactions. However, whatever the field of application, the unstable nature of antioxidants is a problem: The molecules degrade rapidly and have a particularly limited power of action over time.

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Mitochondrial free radical generation, oxidative stress, and aging11This article is dedicated to the memory of our dear friend, colleague, and mentor Lars Ernster (1920–1998), in gratitude for all he gave to us.

Cited by 2,552 publications

References 53 publications

Iron deficiency and iron excess damage mitochondria and mitochondrial DNA in rats

Iron deficiency and iron excess damage mitochondria and mitochondrial DNA in rats

Remarkably high activities of testicular cytochrome c in destroying reactive oxygen species and in triggering apoptosis

One Can Slow Down the Aging through Antioxidants

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