Sex, kings and serial killers and other group-selected human traits

Bowles, Josephine

doi:10.1054/mehy.1999.0951

Cited by 9 publications

(7 citation statements)

References 75 publications

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“…He stressed that, under natural conditions, the majority of organisms die before they become old. Such an assumption is hardly correct since the aging starts long before it appears to be an immediate cause of death 4,6‐8. Indirectly, age‐dependent weakening of an organism can be the reason of death due, for example, to attack by predators, pathogens, etc 4,6‐9.…”

Section: Brief Historymentioning

confidence: 99%

“…Such an assumption is hardly correct since the aging starts long before it appears to be an immediate cause of death 4,6‐8. Indirectly, age‐dependent weakening of an organism can be the reason of death due, for example, to attack by predators, pathogens, etc 4,6‐9. Recently Loison and colleagues10 and Bonduriansky and Brassil11 clearly showed that both long‐lived ungulates (roe deer, bighorn sheep, izards) and the short‐lived antler fly suffer senescence under natural conditions.…”

Section: Brief Historymentioning

confidence: 99%

“…Few years ago, modern proponents of the Wallace‐Weismann concept were very rare 4,6‐8,82,88,104‐108. However, today specialists from various fields of research and different countries are likely to accept such a point of view.…”

Section: Present State Of the Art And Some Perspectivesmentioning

confidence: 99%

“…4,[6][7][8] Indirectly, age-dependent weakening of an organism can be the reason of death due, for example, to attack by predators, pathogens, etc. 4,[6][7][8][9] Recently Loison and colleagues 10 and Bonduriansky and Brassil 11 clearly showed that both longlived ungulates (roe deer, bighorn sheep, izards) and the short-lived antler fly suffer senescence under natural conditions. This is not surprising because a decrease in, for example, skeletal muscle strength starts, as a rule, rather early, that is, at the age when organism stops growing.…”

Section: Brief Historymentioning

confidence: 99%

“…In fact, this observation created the precedent of a signal compound produced by a unicellular eukaryote, which induces death of cells of the same species. Analysis of the mechanism of this effect showed 48,49 that it includes the following consecutive components: (1) pheromone receptor, (2) Ste20 kinase, (3) synthesis of some protein(s), (4) an increase in cytosolic [Ca 2+ ], (5) stimulation of mitochondrial respiration and an increase in energy coupling, (6) a ∆Ψ m elevation, (7) a burst in the ROS production in the middle span of the mitochondrial respiratory chain, (8) decomposition of mitochondrial filaments to small roundish mitochondria, and (9) ∆Ψ m collapse and cytochrome c release from mitochondria to cytosol (FIG. 1).…”

Section: Bacteria and Unicellular Eukaryotesmentioning

confidence: 99%

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Aging as a Mitochondria‐Mediated Atavistic Program: Can Aging Be Switched Off?

Longo

2005

Annals of the New York Academy of Sciences

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Programmed death phenomena have been demonstrated on subcellular (mitoptosis), cellular (apoptosis), and supracellular (collective apoptosis) levels. There are numerous examples of suicide mechanisms at the organismal level (phenoptosis). In yeast, it was recently shown that the death of aging cells is programmed. Many of the steps of programmed cell death are shown to be common for yeast and animals, including mammals. In particular, generation of the mitochondrial reactive oxygen species (ROS) is involved in the suicide programs. Aging of higher animals is accompanied by an increase in damage induced by mitochondrial ROS. Perhaps prevention of such damage by scavenging of mitochondrial ROS might slow down or even switch off the aging programs.

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Section: Brief Historymentioning

confidence: 99%

Section: Brief Historymentioning

confidence: 99%

Section: Present State Of the Art And Some Perspectivesmentioning

confidence: 99%

Section: Brief Historymentioning

confidence: 99%

Section: Bacteria and Unicellular Eukaryotesmentioning

confidence: 99%

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Aging as a Mitochondria‐Mediated Atavistic Program: Can Aging Be Switched Off?

Longo

2005

Annals of the New York Academy of Sciences

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References

2019

Handbook of Crime Correlates

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An attempt to prevent senescence: A mitochondrial approach

Skulachev

Anisimov

Antonenko

et al. 2009

Biochimica et Biophysica Acta (BBA) - Bioenergetics

380

259

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Antioxidants specifically addressed to mitochondria have been studied to determine if they can decelerate senescence of organisms. For this purpose, a project has been established with participation of several research groups from Russia and some other countries. This paper summarizes the first results of the project. A new type of compounds (SkQs) comprising plastoquinone (an antioxidant moiety), a penetrating cation, and a decane or pentane linker has been synthesized. Using planar bilayer phospholipid membrane (BLM), we selected SkQ derivatives with the highest permeability, namely plastoquinonyl-decyl-triphenylphosphonium (SkQ1), plastoquinonyl-decyl-rhodamine 19 (SkQR1), and methylplastoquinonyldecyltriphenylphosphonium (SkQ3). Anti- and prooxidant properties of these substances and also of ubiquinonyl-decyl-triphenylphosphonium (MitoQ) were tested in aqueous solution, detergent micelles, liposomes, BLM, isolated mitochondria, and cell cultures. In mitochondria, micromolar cationic quinone derivatives were found to be prooxidants, but at lower (sub-micromolar) concentrations they displayed antioxidant activity that decreases in the series SkQ1=SkQR1>SkQ3>MitoQ. SkQ1 was reduced by mitochondrial respiratory chain, i.e. it is a rechargeable antioxidant. Nanomolar SkQ1 specifically prevented oxidation of mitochondrial cardiolipin. In cell cultures, SkQR1, a fluorescent SkQ derivative, stained only one type of organelles, namely mitochondria. Extremely low concentrations of SkQ1 or SkQR1 arrested H(2)O(2)-induced apoptosis in human fibroblasts and HeLa cells. Higher concentrations of SkQ are required to block necrosis initiated by reactive oxygen species (ROS). In the fungus Podospora anserina, the crustacean Ceriodaphnia affinis, Drosophila, and mice, SkQ1 prolonged lifespan, being especially effective at early and middle stages of aging. In mammals, the effect of SkQs on aging was accompanied by inhibition of development of such age-related diseases and traits as cataract, retinopathy, glaucoma, balding, canities, osteoporosis, involution of the thymus, hypothermia, torpor, peroxidation of lipids and proteins, etc. SkQ1 manifested a strong therapeutic action on some already pronounced retinopathies, in particular, congenital retinal dysplasia. With drops containing 250 nM SkQ1, vision was restored to 67 of 89 animals (dogs, cats, and horses) that became blind because of a retinopathy. Instillation of SkQ1-containing drops prevented the loss of sight in rabbits with experimental uveitis and restored vision to animals that had already become blind. A favorable effect of the same drops was also achieved in experimental glaucoma in rabbits. Moreover, the SkQ1 pretreatment of rats significantly decreased the H(2)O(2) or ischemia-induced arrhythmia of the isolated heart. SkQs strongly reduced the damaged area in myocardial infarction or stroke and prevented the death of animals from kidney ischemia. In p53(-/-) mice, 5 nmol/kgxday SkQ1 decreased the ROS level in the spleen and inhibited appearance of lymphomas to th...

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Sex, kings and serial killers and other group-selected human traits

Cited by 9 publications

References 75 publications

Aging as a Mitochondria‐Mediated Atavistic Program: Can Aging Be Switched Off?

Aging as a Mitochondria‐Mediated Atavistic Program: Can Aging Be Switched Off?

References

An attempt to prevent senescence: A mitochondrial approach

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