akhusker
01-13-2012, 07:08 AM
Secrets of L-Carnosine
"When I first studied and took supplemental carnosine two years ago, immediately I thought of the implications for the aging bodybuilderdue to carnosine's effects on bodily proteins which are staggering.I began studying antioxidants and anti-glycation agents awhile before that and was eventually introduced to carnosine. It only made sense to me that carnosine might be of interest to bodybuilders, since it inhibits many pathways specific to the destruction and malfunction of bodily proteins. These may be key issues for bodybuilders who wish to make continued progress in the form of acquiring and maintaining mature, healthy, lean body mass into middle age and beyond.
Carnosine is a naturally occurring, multifunctional dipeptide comprised of the amino acids beta-alanine and l-histidine. Carnosine is largely present in skeletal muscle. Carnosine provides excellent pH buffering capacity of skeletal muscle during training. White muscle fibers contain higher levels of carnosine where anaerobic metabolism is frequent in the weight training enthusiast. Carnosine protects skeletal muscle membranes by inhibiting lipid peroxidation. As you know, the cellular membranes of the mitochondria in skeletal muscle are largely comprised of a delicate balance of fatty acids. Oxidation primarily takes place via the polyunsaturated fatty acids. Carnosine inhibits this destructive process that is catalyzed by numerous pathways and does so in measurable quantity. The impact of carnosine's lipid peroxidation inhibiting (antioxidant) activity is concentration dependant in skeletal muscle. In human skeletal muscle, carnosine levels decline significantly with age in measurably predictable amounts. This brings a decline in the antioxidant activities of carnosine which may result in some functional deterioration and structural changes in skeletal muscle. This lack of antioxidant protection for the cellular membranes of skeletal muscle cells may work in concert with specific atrophic mechanisms associated with biological aging. Many catalysts of lipid peroxidation and free radicals are found in the cytostolic environment (inside the cytoplasm of the cell, the mitochondria). Fortunately, the hydrophilic (water loving) nature of carnosine provides protection here. Besides free radical scavenging, the metal chelating actions of carnosine are thought to be responsible for it's protective antioxidant effects. Sometimes there may be a build up (too much) of heavy metals in the human organism. Carnosine forms a whole new compound with certain highly reactive metals which cause toxicity through free radical activity. These newly formed "chelate compounds" turn the tables on heavy metal toxicity by scavenging and effectively quenching powerful free radicals such as singlet oxygen and superoxide anion radicals. Also, when carnosine combines with certain metals such as copper, it decreases the reactivity of the metal itself, making it's very presence less of a burden in terms of "side effects." I've always viewed a "side effect" as a peripheral consequence produced in the pursuit (means) of a specific and desirable outcome (ends). Sometimes the means does not always justify the ends which I call the "risk to benefit ratio." See, many trace metals are very necessary for human life and function, but there can be undesirable reactions the body has to even their very presence in varying amounts. I learned the concept of action/reaction from Author L. Rea's reading materials in an attempt to create a superior anabolic environment inside my body. He taught me that for every action there is a reaction (good and bad). Every technique, supplement, etc, that is administered in the human body which brings progress is a two edged sword. Knowing how to effectively act upon a negative reaction by your body to a step made in the right direction is the key to continual progress. What goes on inside the human body without any help from us is no different. This is the paradox, the essence of biological life itself which I will touch on in a moment. Carnosine "intercepts" the bad consequences of many negative reactions to the basic (good) processes of daily metabolism necessary for life and function.
The age of a human serves as a negative indicator of free carnosine concentrations in skeletal muscle. A decline in free concentrations of 63% occurs in human subjects between the ages of 10 an 70. So a strong association exists between decreased skeletal muscle strength and function and decreased tissue concentration of carnosine as humans age. The great biochemical parodox of life I mentioned is that the essential elements necessary for the creation and maintenance of biological life (trace metals, lipids, oxygen glucose, proteins) also destroy life. They give us life and systematically kill us. Many of the ways they kill us are inhibited by carnosine. Skeletal muscle and the entire human body is comprised mostly of proteins. As we age, these proteins undergo destructive changes such as oxidation (previously mentioned) and interactions with sugars or aldehydes. A major cause of these negative protein modifications is the formation of advanced glycation end products (AGE's). There are tell tale signs we are all familiar with such as neurodegeneration, cataract formation and those unattractive "age spots" you see on middle aged to elderly humans. "AGE" is somewhat of a suitable acronym in this instance, because growing old is the affecting association we observe. Powerfully negative protein modifications inhibited by carnosine include AGE formation, glycation, protein cross linking, carbonylation, oxidation and trace metal toxicity.
Carnosine also has a remarkable ability to rejuvenate connective tissue cells by prolonging cellular senescence ( a twilight state I think of metaphorically as approaching the end of the day or dusk) which denotes the end of the life cycle of cellular division. All cells have a limited capacity to divide through the course of life. The end of cellular division results in apoptosis (programmed cellular death). This limited capacity of cells to promote themselves by dividing is called the "Hayflick Limit," after the scientist who discovered it. Telomeres count off the rounds of cell division as the Hayflick Limit caps life span at the level of the cell. Telomeres shorten as the cells' ability to divide themselves decreases. Some people postulate that telomeres are a form of a "biological clock" that determines lifespan. The more cells divide, the chances of them dividing again decreases until division stops altogether and each cell becomes senescent. As cultured human fibroblasts (connective tissue cells) approached the Hayflick Limit in some remarkable laboratory experiments, they became irregular in shape and formed or assumed a distorted appearance called the "senescent phenotype," before cellular division ceased. These scientists at an Australian research institute discovered that these cultured human cells, (fibroblasts), after many rounds of division, (late passage cells), when exposed to carnosine, were rejuvenated, lived longer, and retained youthful appearance and growth patterns. When these late-passage fibroblasts were transferred back to a culture medium without the presence of carnosine, the observable evidence of senescence quickly reappeared. This was done several times with consistent results.
Also, these cells often exhibited an enhanced capacity to divide. Even when originally old cells were exposed to carnosine life span was increased. When cells in the carnosine medium eventually did enter into senescence, they retained a normal morphology. I should include that the chronological life span of old cells were more dramatically increased than cellular hyperplasia or "population doublings" in the Australian studies. So, carnosine's ability to retain and even regain the "youthful phenotype" is indicative of a positive influence on cellular homeostasis. Carnosine improves post surgical wound healing. Skin aging is all tied up in negative protein modification. Damaged proteins build up and cross link as they interact with sugars causing wrinkles and the loss of elasticity. That alone is cosmetically bad for a bodybuilder. The reason why older folks look different than us younger people is due to changes in the proteins of the body.
Proteins (amino acids) are the building blocks of life. I learned that in seventh grade Biology 101. Proteins are most responsible for the routine functions within living organisms. This is why the deterioration of bodily proteins have such a fundamental impact on the body's function and appearance. A huge central factor in the negative structural changes of bodily proteins is called "glycation." Glycation is a result of undesirable reactions between sugars in the body and it's proteins. These modified protein structures accumulate inside the human body as carnosine levels decline. Once modified in this way, a protein loses it's ability to function properly. As these modified proteins increase in number throughout the body, a person becomes more susceptible to degenerative diseases. Obviously, these damaged proteins, given time, indicate significant losses in skeletal muscle structure and function for the aging bodybuilder. Also, imagine the impact on neural and vascular support networks necessary to grow and maintain skeletal muscle size and strength. Then there are all the hormonal receptor sites throughout the body we depend on to receive chemical messages and deliver them or to transport substances such as amino acids, glucose and fatty acids inside muscle cells to promote anabolism/lipolysis. AGE formation in the body is not unlike the browning of food in an oven. This is irreversable. Once proteins build up AGEs they do turn brown. Remember, "age spots?" AGE formation cross links proteins to the point where the metabolism cannot break them down. This reduces and slows overall cellular turnover (division) within the body. Tissues lose elasticity, resiliency, and organ systems degenerate as AGEs accumulate in the body. One example is the deteriorization of the cardiovascular system with AGEs now being a major player. I believe skin aging (the body's largest and most visible organ) is another. Just imagine how horribly AGEs affect skeletal muscle as we humans age.
Personally, it hurts me to think about it. Therefore, I do what I can to prevent it through supplementation. Carnosine has demonstrated itself to be, by far, the safest and most effective, natural anti-glycating agent known to man. If there is something better, I don't know about it. I know that keeping insulin sensitivity as high as possible at all times is incredibly helpful through maximizing efficient glucose disposal. However, I'm talking about a naturally occurring neutraceutical that can be exogeneously consumed. Receptors for AGEs have rightfully been recognized as RAGEs (receptors for glycation end products). When AGEs bind with their receptors, (RAGEs), I want to mention that one consequence is a fifty-fold increase in free radical generation. Can you say "explosion?" Through it's structural resemblence to these AGE receptor sites, (which AGEs bind to), carnosine acts as a "sacrificial landfill." By becoming glycated itself, carnosine spares bodily proteins the same fate. This new substance, glycated carnosine, minds it's own business by being non-mutagenic (does not multiply or spread), unlike some bodily proteins. So not only does carnosine inhibit the formation of AGEs, it helps protect normal (undamaged protein) from the toxic effects of AGEs that have already formed. Carnosine has proven itself able to inhibit the cross linking of damaged proteins (by AGEs) with healthy ones, preventing the spread of damaged proteins while promoting the disposal of damaged, unuseable proteins. There are multiple pathways of negative protein modification that are beyond the scope of this article and simply just antioxidant protection. However, the last huge one I must mention is the carbonylation of bodily proteins. This is a very destructive process and carnosine inhibits the major pathways through which proteins are carbonylated. These include carnosine's ability to protect proteins via it's anti- glycation and antioxidant affects, it's ability to quench reactive aldehydes, chelate metals and protect against lipid peroxidation. It does all this shockingly well. Carnosine removes the carbonyl groups in glycated proteins. This does stop existing protein damage from spreading to healthy proteins.
There are so many other health benefits of supplemental carnosine for the bodybuilder or anyone else, but I'm going to draw this article to a close. I've attempted to draw attention to the implications of carnosine's protective effect on the structural integrity and function of the skeletal muscle cells, (can you say "protein?"), including hormonal receptor sites (protein) throughout the human body. Although the overall health benefits of supplementation are profound, I thought possibly that it's symbiotic (mutually beneficial) relationship with bodily proteins would provoke some interest and thought. I find it rather fascinating. I did not get into brain neurotransmitters, Alzheimers disease, etc.... I tried to stick to the "physical" implications for bodybuilders and how carnosine can protect our health and helpensure our hard work as we approach middle age and beyond. All animal, mice, rat studies, etc, that I've read are congruent with the protective, preserving and many positive effects of carnosine in human cells, both in vivo and outside the laboratory.
Bauer, K., and Schulz, M. (1994) Eur. J. Biochem., 219, 43-47.
Davey, C. L. (1960) Arch. Biochem. Biophys., 89, 303.
Harris, R. C., Marlin, D. J., Dunnett, M., Snow, D. H., and
Hultmann, E. (1990) Comp. Biochem. Physiol., 97, 249-251.
Boldyrev, A. A., Dupin, A. M., Pindel, E. V., and Severin, S. E.
(1988) Comp. Biochem. Physiol., 89, 245.
Rubtsov, A. M., Schara, M., Sentiurc, M., and Boldyrev, A. A.
(1991) Acta Pharm. Jugosl., 41, 401.
Dahl, T. A., Midden, W. R., and Hartmann, P. E. (1988) Photochem.
Photobiol., 47, 357.
Decker, E. A., and Faraji, H. (1990) JAOCS, 67, 650.
Kohen, R., Yamamoto, Y., Cundy, K. C., and Ames, B. N. (1988) Proc.
Natl. Acad. Sci. USA, 85, 3175-3179.
Yoshikawa, T., Naito, Y., Tanigawa, T., Yoneta, T., and Kondo, M.
(1991) Biochim. Biophys. Acta, 115, 15-20.
Yoshikawa, T., Naito, Y., Tanigawa, T., Yoneta, T., Yasuda, M.,
Ueda, S., Oyamada, H., and Kondo, M. (1991) Free Rad. Res. Commun.,
14, 289-296.
Berlett BS, Stadtman ER. Protein oxidation in aging, disease, and
oxidative stress. J Biol Chem. 1997; 272(33):20313-6.
Bierhaus A, Hofmann MA, Ziegler R, et al. AGEs and their
interaction with AGE-receptors in vascular disease and diabetes
mellitus. I. The AGE concept. Cardiovascular Research. 1998;
37(3):586-600.
Brownson C, Hipkiss AR. Carnosine reacts with a glycated protein.
Free Radic Biol Med. 2000; 28(10):1564-70.
Granstrom, Karin J. Carnosine Nature's Pluripotent Life Extension
Agent. Life Extension Magazine. 2001; Cover story.
Hayflick L. The limited in vitro lifetime of human diploid cell
strains. Exp Cell Res. 1965; 37:614-36.
Hayflick L, Moorhead PS. The serial cultivation of human diploid
cell strains. Exp Cell Res. 1961; 25:585-621.
Hipkiss AR, Michaelis J, Syrris P, et al. Strategies for the
extension of human life span. Perspect Hum Biol. 1995; 1:59-70.
McFarland GA, Holliday R. Retardation of the senescence of cultured
human diploid fibroblasts by carnosine. Exp Cell Res 1994;
212(2):167-75.
McFarland GA, Holliday R. Further evidence for the rejuvenating
effects of the dipeptide L-carnosine on cultured human diploid
fibroblasts. Exp Gerontol. 1999; 34(1):35-45.
Preston JE, Hipkiss AR, Himsworth DT, et al. Toxic effects of beta-
amyloid(25-35) on immortalised rat brain endothelial cell:
protection by carnosine, homocarnosine and beta-alanine. Neurosci
Lett. 1998; 242(2):105-8.
Quinn PJ, Boldyrev AA, Formazuyk VE. Carnosine: its properties,
functions and potential therapeutic applications. Mol Aspects Med.
1992; 13(5):379-444.
Schmidt AM, Yan SD, Wautier JL, et al. Activation of receptor for
advanced glycation end products: a mechanism for chronic vascular
dysfunction in diabetic vasculopathy and atherosclerosis. Circ Res.
1999; 84(5):489-97.
Stadtman ER. Protein oxidation and aging. Science. 1992;
257(5074):1220-4.
Stadtman ER, Levine RL. Protein oxidation. Ann NY Acad Sci. 2000;
899:191-208.
Stuerenburg, H.J. The Roles of Carnosine in Aging of Skeletal
Muscle and in Neuromuscular Diseases. Biochemistry (Moscow), Vol
65, No. 7, 2000, pp. 862-865. Translated from Biokhimiya, Vol. 65,
No. 7, 2000, pp. 1013-1017. Original Russian Text Copyright 2000 by
Stuerenburg."
Written By ClarityandFocus
Please credit this work if it is to be reposted
"When I first studied and took supplemental carnosine two years ago, immediately I thought of the implications for the aging bodybuilderdue to carnosine's effects on bodily proteins which are staggering.I began studying antioxidants and anti-glycation agents awhile before that and was eventually introduced to carnosine. It only made sense to me that carnosine might be of interest to bodybuilders, since it inhibits many pathways specific to the destruction and malfunction of bodily proteins. These may be key issues for bodybuilders who wish to make continued progress in the form of acquiring and maintaining mature, healthy, lean body mass into middle age and beyond.
Carnosine is a naturally occurring, multifunctional dipeptide comprised of the amino acids beta-alanine and l-histidine. Carnosine is largely present in skeletal muscle. Carnosine provides excellent pH buffering capacity of skeletal muscle during training. White muscle fibers contain higher levels of carnosine where anaerobic metabolism is frequent in the weight training enthusiast. Carnosine protects skeletal muscle membranes by inhibiting lipid peroxidation. As you know, the cellular membranes of the mitochondria in skeletal muscle are largely comprised of a delicate balance of fatty acids. Oxidation primarily takes place via the polyunsaturated fatty acids. Carnosine inhibits this destructive process that is catalyzed by numerous pathways and does so in measurable quantity. The impact of carnosine's lipid peroxidation inhibiting (antioxidant) activity is concentration dependant in skeletal muscle. In human skeletal muscle, carnosine levels decline significantly with age in measurably predictable amounts. This brings a decline in the antioxidant activities of carnosine which may result in some functional deterioration and structural changes in skeletal muscle. This lack of antioxidant protection for the cellular membranes of skeletal muscle cells may work in concert with specific atrophic mechanisms associated with biological aging. Many catalysts of lipid peroxidation and free radicals are found in the cytostolic environment (inside the cytoplasm of the cell, the mitochondria). Fortunately, the hydrophilic (water loving) nature of carnosine provides protection here. Besides free radical scavenging, the metal chelating actions of carnosine are thought to be responsible for it's protective antioxidant effects. Sometimes there may be a build up (too much) of heavy metals in the human organism. Carnosine forms a whole new compound with certain highly reactive metals which cause toxicity through free radical activity. These newly formed "chelate compounds" turn the tables on heavy metal toxicity by scavenging and effectively quenching powerful free radicals such as singlet oxygen and superoxide anion radicals. Also, when carnosine combines with certain metals such as copper, it decreases the reactivity of the metal itself, making it's very presence less of a burden in terms of "side effects." I've always viewed a "side effect" as a peripheral consequence produced in the pursuit (means) of a specific and desirable outcome (ends). Sometimes the means does not always justify the ends which I call the "risk to benefit ratio." See, many trace metals are very necessary for human life and function, but there can be undesirable reactions the body has to even their very presence in varying amounts. I learned the concept of action/reaction from Author L. Rea's reading materials in an attempt to create a superior anabolic environment inside my body. He taught me that for every action there is a reaction (good and bad). Every technique, supplement, etc, that is administered in the human body which brings progress is a two edged sword. Knowing how to effectively act upon a negative reaction by your body to a step made in the right direction is the key to continual progress. What goes on inside the human body without any help from us is no different. This is the paradox, the essence of biological life itself which I will touch on in a moment. Carnosine "intercepts" the bad consequences of many negative reactions to the basic (good) processes of daily metabolism necessary for life and function.
The age of a human serves as a negative indicator of free carnosine concentrations in skeletal muscle. A decline in free concentrations of 63% occurs in human subjects between the ages of 10 an 70. So a strong association exists between decreased skeletal muscle strength and function and decreased tissue concentration of carnosine as humans age. The great biochemical parodox of life I mentioned is that the essential elements necessary for the creation and maintenance of biological life (trace metals, lipids, oxygen glucose, proteins) also destroy life. They give us life and systematically kill us. Many of the ways they kill us are inhibited by carnosine. Skeletal muscle and the entire human body is comprised mostly of proteins. As we age, these proteins undergo destructive changes such as oxidation (previously mentioned) and interactions with sugars or aldehydes. A major cause of these negative protein modifications is the formation of advanced glycation end products (AGE's). There are tell tale signs we are all familiar with such as neurodegeneration, cataract formation and those unattractive "age spots" you see on middle aged to elderly humans. "AGE" is somewhat of a suitable acronym in this instance, because growing old is the affecting association we observe. Powerfully negative protein modifications inhibited by carnosine include AGE formation, glycation, protein cross linking, carbonylation, oxidation and trace metal toxicity.
Carnosine also has a remarkable ability to rejuvenate connective tissue cells by prolonging cellular senescence ( a twilight state I think of metaphorically as approaching the end of the day or dusk) which denotes the end of the life cycle of cellular division. All cells have a limited capacity to divide through the course of life. The end of cellular division results in apoptosis (programmed cellular death). This limited capacity of cells to promote themselves by dividing is called the "Hayflick Limit," after the scientist who discovered it. Telomeres count off the rounds of cell division as the Hayflick Limit caps life span at the level of the cell. Telomeres shorten as the cells' ability to divide themselves decreases. Some people postulate that telomeres are a form of a "biological clock" that determines lifespan. The more cells divide, the chances of them dividing again decreases until division stops altogether and each cell becomes senescent. As cultured human fibroblasts (connective tissue cells) approached the Hayflick Limit in some remarkable laboratory experiments, they became irregular in shape and formed or assumed a distorted appearance called the "senescent phenotype," before cellular division ceased. These scientists at an Australian research institute discovered that these cultured human cells, (fibroblasts), after many rounds of division, (late passage cells), when exposed to carnosine, were rejuvenated, lived longer, and retained youthful appearance and growth patterns. When these late-passage fibroblasts were transferred back to a culture medium without the presence of carnosine, the observable evidence of senescence quickly reappeared. This was done several times with consistent results.
Also, these cells often exhibited an enhanced capacity to divide. Even when originally old cells were exposed to carnosine life span was increased. When cells in the carnosine medium eventually did enter into senescence, they retained a normal morphology. I should include that the chronological life span of old cells were more dramatically increased than cellular hyperplasia or "population doublings" in the Australian studies. So, carnosine's ability to retain and even regain the "youthful phenotype" is indicative of a positive influence on cellular homeostasis. Carnosine improves post surgical wound healing. Skin aging is all tied up in negative protein modification. Damaged proteins build up and cross link as they interact with sugars causing wrinkles and the loss of elasticity. That alone is cosmetically bad for a bodybuilder. The reason why older folks look different than us younger people is due to changes in the proteins of the body.
Proteins (amino acids) are the building blocks of life. I learned that in seventh grade Biology 101. Proteins are most responsible for the routine functions within living organisms. This is why the deterioration of bodily proteins have such a fundamental impact on the body's function and appearance. A huge central factor in the negative structural changes of bodily proteins is called "glycation." Glycation is a result of undesirable reactions between sugars in the body and it's proteins. These modified protein structures accumulate inside the human body as carnosine levels decline. Once modified in this way, a protein loses it's ability to function properly. As these modified proteins increase in number throughout the body, a person becomes more susceptible to degenerative diseases. Obviously, these damaged proteins, given time, indicate significant losses in skeletal muscle structure and function for the aging bodybuilder. Also, imagine the impact on neural and vascular support networks necessary to grow and maintain skeletal muscle size and strength. Then there are all the hormonal receptor sites throughout the body we depend on to receive chemical messages and deliver them or to transport substances such as amino acids, glucose and fatty acids inside muscle cells to promote anabolism/lipolysis. AGE formation in the body is not unlike the browning of food in an oven. This is irreversable. Once proteins build up AGEs they do turn brown. Remember, "age spots?" AGE formation cross links proteins to the point where the metabolism cannot break them down. This reduces and slows overall cellular turnover (division) within the body. Tissues lose elasticity, resiliency, and organ systems degenerate as AGEs accumulate in the body. One example is the deteriorization of the cardiovascular system with AGEs now being a major player. I believe skin aging (the body's largest and most visible organ) is another. Just imagine how horribly AGEs affect skeletal muscle as we humans age.
Personally, it hurts me to think about it. Therefore, I do what I can to prevent it through supplementation. Carnosine has demonstrated itself to be, by far, the safest and most effective, natural anti-glycating agent known to man. If there is something better, I don't know about it. I know that keeping insulin sensitivity as high as possible at all times is incredibly helpful through maximizing efficient glucose disposal. However, I'm talking about a naturally occurring neutraceutical that can be exogeneously consumed. Receptors for AGEs have rightfully been recognized as RAGEs (receptors for glycation end products). When AGEs bind with their receptors, (RAGEs), I want to mention that one consequence is a fifty-fold increase in free radical generation. Can you say "explosion?" Through it's structural resemblence to these AGE receptor sites, (which AGEs bind to), carnosine acts as a "sacrificial landfill." By becoming glycated itself, carnosine spares bodily proteins the same fate. This new substance, glycated carnosine, minds it's own business by being non-mutagenic (does not multiply or spread), unlike some bodily proteins. So not only does carnosine inhibit the formation of AGEs, it helps protect normal (undamaged protein) from the toxic effects of AGEs that have already formed. Carnosine has proven itself able to inhibit the cross linking of damaged proteins (by AGEs) with healthy ones, preventing the spread of damaged proteins while promoting the disposal of damaged, unuseable proteins. There are multiple pathways of negative protein modification that are beyond the scope of this article and simply just antioxidant protection. However, the last huge one I must mention is the carbonylation of bodily proteins. This is a very destructive process and carnosine inhibits the major pathways through which proteins are carbonylated. These include carnosine's ability to protect proteins via it's anti- glycation and antioxidant affects, it's ability to quench reactive aldehydes, chelate metals and protect against lipid peroxidation. It does all this shockingly well. Carnosine removes the carbonyl groups in glycated proteins. This does stop existing protein damage from spreading to healthy proteins.
There are so many other health benefits of supplemental carnosine for the bodybuilder or anyone else, but I'm going to draw this article to a close. I've attempted to draw attention to the implications of carnosine's protective effect on the structural integrity and function of the skeletal muscle cells, (can you say "protein?"), including hormonal receptor sites (protein) throughout the human body. Although the overall health benefits of supplementation are profound, I thought possibly that it's symbiotic (mutually beneficial) relationship with bodily proteins would provoke some interest and thought. I find it rather fascinating. I did not get into brain neurotransmitters, Alzheimers disease, etc.... I tried to stick to the "physical" implications for bodybuilders and how carnosine can protect our health and helpensure our hard work as we approach middle age and beyond. All animal, mice, rat studies, etc, that I've read are congruent with the protective, preserving and many positive effects of carnosine in human cells, both in vivo and outside the laboratory.
Bauer, K., and Schulz, M. (1994) Eur. J. Biochem., 219, 43-47.
Davey, C. L. (1960) Arch. Biochem. Biophys., 89, 303.
Harris, R. C., Marlin, D. J., Dunnett, M., Snow, D. H., and
Hultmann, E. (1990) Comp. Biochem. Physiol., 97, 249-251.
Boldyrev, A. A., Dupin, A. M., Pindel, E. V., and Severin, S. E.
(1988) Comp. Biochem. Physiol., 89, 245.
Rubtsov, A. M., Schara, M., Sentiurc, M., and Boldyrev, A. A.
(1991) Acta Pharm. Jugosl., 41, 401.
Dahl, T. A., Midden, W. R., and Hartmann, P. E. (1988) Photochem.
Photobiol., 47, 357.
Decker, E. A., and Faraji, H. (1990) JAOCS, 67, 650.
Kohen, R., Yamamoto, Y., Cundy, K. C., and Ames, B. N. (1988) Proc.
Natl. Acad. Sci. USA, 85, 3175-3179.
Yoshikawa, T., Naito, Y., Tanigawa, T., Yoneta, T., and Kondo, M.
(1991) Biochim. Biophys. Acta, 115, 15-20.
Yoshikawa, T., Naito, Y., Tanigawa, T., Yoneta, T., Yasuda, M.,
Ueda, S., Oyamada, H., and Kondo, M. (1991) Free Rad. Res. Commun.,
14, 289-296.
Berlett BS, Stadtman ER. Protein oxidation in aging, disease, and
oxidative stress. J Biol Chem. 1997; 272(33):20313-6.
Bierhaus A, Hofmann MA, Ziegler R, et al. AGEs and their
interaction with AGE-receptors in vascular disease and diabetes
mellitus. I. The AGE concept. Cardiovascular Research. 1998;
37(3):586-600.
Brownson C, Hipkiss AR. Carnosine reacts with a glycated protein.
Free Radic Biol Med. 2000; 28(10):1564-70.
Granstrom, Karin J. Carnosine Nature's Pluripotent Life Extension
Agent. Life Extension Magazine. 2001; Cover story.
Hayflick L. The limited in vitro lifetime of human diploid cell
strains. Exp Cell Res. 1965; 37:614-36.
Hayflick L, Moorhead PS. The serial cultivation of human diploid
cell strains. Exp Cell Res. 1961; 25:585-621.
Hipkiss AR, Michaelis J, Syrris P, et al. Strategies for the
extension of human life span. Perspect Hum Biol. 1995; 1:59-70.
McFarland GA, Holliday R. Retardation of the senescence of cultured
human diploid fibroblasts by carnosine. Exp Cell Res 1994;
212(2):167-75.
McFarland GA, Holliday R. Further evidence for the rejuvenating
effects of the dipeptide L-carnosine on cultured human diploid
fibroblasts. Exp Gerontol. 1999; 34(1):35-45.
Preston JE, Hipkiss AR, Himsworth DT, et al. Toxic effects of beta-
amyloid(25-35) on immortalised rat brain endothelial cell:
protection by carnosine, homocarnosine and beta-alanine. Neurosci
Lett. 1998; 242(2):105-8.
Quinn PJ, Boldyrev AA, Formazuyk VE. Carnosine: its properties,
functions and potential therapeutic applications. Mol Aspects Med.
1992; 13(5):379-444.
Schmidt AM, Yan SD, Wautier JL, et al. Activation of receptor for
advanced glycation end products: a mechanism for chronic vascular
dysfunction in diabetic vasculopathy and atherosclerosis. Circ Res.
1999; 84(5):489-97.
Stadtman ER. Protein oxidation and aging. Science. 1992;
257(5074):1220-4.
Stadtman ER, Levine RL. Protein oxidation. Ann NY Acad Sci. 2000;
899:191-208.
Stuerenburg, H.J. The Roles of Carnosine in Aging of Skeletal
Muscle and in Neuromuscular Diseases. Biochemistry (Moscow), Vol
65, No. 7, 2000, pp. 862-865. Translated from Biokhimiya, Vol. 65,
No. 7, 2000, pp. 1013-1017. Original Russian Text Copyright 2000 by
Stuerenburg."
Written By ClarityandFocus
Please credit this work if it is to be reposted