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Mitochondria, the power plants of the cell, generate reactive oxygen species (ROS) as a side effect of the energetic operations needed to package fuel supplies used by cellular processes. While ROS are necessary signals in many physiological circumstances, such as the beneficial reaction to exercise, excessive ROS generation can be harmful. Excessive ROS generation is also observed in aging. Suppressing that excessive ROS flux at its source, without affecting the beneficial signaling roles, has been demonstrated to be beneficial in disease states characterized by inflammation and high degrees of oxidative stress. It may also very modestly slow the progression of aging.
A number of mitochondrially targeted antioxidant compounds have been developed over the past fifteen years, and shown to produce at least some these benefits: MitoQ, SkQ1, SS31, and so forth. An alternative approach to delivering antioxidants to the mitochondria, to soak up ROS as they are generated, is to suppress the production of ROS. The challenge here is doing this without disrupting the normal function of mitochondria, which would of course be far more damaging than any potential realized benefit.
Regardless, a small class of mitochondrial ROS blocker compounds does exist, and here researchers show that the approved drug anethole trithione, also known as sulfarlem, and in this paper, confusingly, by the designation OP2113, is also a mitochondrial ROS blocker. It can achieve this goal without greatly altering mitochondrial function. It remains to be seen as to whether this compound can do as well as mitochondrially targeted antioxidants, should it or an improved version be further developed for this clinical use. It is worth remembering that even it it does, and can improve health to some degree, as suggested by human clinical trials, the effects on longevity will be vanishingly small in long-lived species such as our own. They are not large in flies or mice, species with a far greater plasticity of longevity.
The free radical theory of aging suggests that free radical-induced damage to cellular structures is a crucial event in aging; however, clinical trials on antioxidant supplementation in various populations have not successfully demonstrated an anti-aging effect. Current explanations include the lack of selectivity of available antioxidants for the various sources of oxygen radicals and the poor distribution of antioxidants to mitochondria, which are now believed to be both the primary sources of reactive oxygen species (ROS) and primary targets of ROS-induced damage. Indeed, mitochondrial dysfunction that occurs due to accumulation of oxidative damage is implicated in the pathogenesis of virtually all human age-related diseases.
Given the key role of age-dependent mitochondrial deterioration in aging, there is currently a great interest in approaches to protect mitochondria from ROS-mediated damage. Mitochondria are not only a major source of ROS but also particularly susceptible to oxidative damage. Consequently, mitochondria accumulate oxidative damage with age that contribute to mitochondrial dysfunction. Cells and even organelles possess several protection pathways against this ROS-mediated damage given that local protection is fundamental to circumvent the high reactivity of ROS. Therefore, mitochondria appear as the main victims of their own ROS production, and evidence suggests that the best mitochondrial protection will be obtained from inside mitochondria.
his conclusion has driven several potential therapeutic strategies to improve mitochondrial function in aging and pathologies. Antioxidants designed for accumulation by mitochondria in vivo have been developed and are currently being thoroughly tested for mitochondrial protection. The growing interest in ROS production associated with diseases has elicited numerous clinical trials that have also demonstrated that uncontained ROS reduction in cells is deleterious, and it appears that an adequate balance of ROS production is necessary for correct cell function. As a consequence, there is also a growing interest in the selective inhibition of ROS production of mitochondrial origin that would not affect cellular signalization involving either mitochondrial or cytosolic ROS production.
The molecule OP2113 (Anetholtrithion, or 5-(4-methoxyphenyl)dithiole-3-thione, CAS number 532-11-6) has been marketed in many countries and used in human therapy in certain countries including France, Germany, and China for its choleretic and sialogogic properties. Anetholtrithion also exhibits chemoprotective effects against cancer and various kinds of toxicity caused by some drugs and xenobiotics. These chemoprotective effects appear to be mainly due to its antioxidant properties. The most typical indications for which anetholtrithion is currently used include increasing salivary secretion in patients experiencing dry mouth.
However, until now, no precise mechanism of action has been described for this molecule. Considering the high lipophilicity of OP2113, which represents a promising characteristic for mitochondrial targeting, we investigated the effect of OP2113 on mitochondrial ROS/H2O2 production. Here we show that OP2113 decreases ROS/H2O2 production by isolated rat heart mitochondria. Interestingly, it does not act as an unspecific antioxidant molecule, but as a direct specific inhibitor of ROS production at complex I of the mitochondrial respiratory chain, without impairing electron transfer. This work represents the first demonstration of a drug authorized for use in humans that can prevent mitochondria from producing ROS/H2O2.
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