Although taurine supplementation enhances exercise performance, its efflux during exercise and/or ischemia, with consequent decrease in tissue concentration, can also occur [60, 61]. Whether the loss of taurine is a marker of tissue damage or rather a cytoprotective mechanism against ischemic insult, is still matter of debate [60, 62, 63].
Continued intake of 2.7% methionine for up to 20 d led to erythrocyte engorgement and hemosiderin accumulation, depression of growth, and liver damage (86). In piglets fed various dl-methionine levels up to 4% of the diet for 27 d, the plasma methionine concentration increased to 100 times the basal level at the highest intake (87).
The efflux of taurine during exercise and/or ischemia may be required to relief a basal inhibitory effect and to enhance the potassium efflux and membrane repolarization via the specific channels activated by ATP depletion and/or intracellular calcium accumulation. This would exert a protective action against exercise-induced fatigue or impairment in muscle performance related to ischemia-reperfusion injury [64, 65].
2. As far as inherited or acquired pathophysiological conditions of skeletal muscle are concerned, the pre-clinical findings allow to distinguish effects related to exogenous pharmacological action of taurine on rather specific targets, such as in myotonic syndromes, to conditions that may be accompanied by changes in intercellular taurine content or change in calcium homeostasis, in which a taurine supplementation may be helpful to restore altered levels. Skeletal muscle is one of the tissues able to concentrate the largest amount of bodyâ€™s taurine, via the TauT activity.
A decrease in markers of oxidative stress was also found, indicating that taurine may help to control activity-related oxidative stress . In support to this view, a recent report by Silva et al. showed that a daily treatment of rats with 300 mg/kg taurine for 2 weeks protects muscles against in vivo eccentric exercise damage, such as downhill running . In particular taurine reduced protein carbonylation or oxidized thiols, without increasing the expression of endogenous anti-oxidant pathways, such as superoxide dismutase or catalase .
Construction of transgenic mice expressing Î”23-134 PrP
However, more information is needed to know the significance of this interaction. Branched-chain amino acids might decrease blood sugar.
Long-term liver damage (liver cirrhosis). It is not clear if branched-chain amino acids benefit people with liver cirrhosis.
- Reduced plasma copper was also reported, and the hypercholesterolemia was reversed by dietary copper supplementation (71).
- The protective effect of taurine efflux in the above conditions can be related to the need to osmotically balance, along with water movement, the increase of by-products of metabolism in the myofibers [1, 14].
- Taurine muscle levels were not assessed, thus the correlation between taurine effect and a specific muscle action is rather indirect.
Other evidences support that the sulfonic amino acid is actually incapable of scavenging the common oxidants, namely, superoxide, hydrogen peroxide and hydroxyl radical, which instead are the main products of enhanced NADPH oxidase activity in dystrophic muscle [99-101]. However, the amino group of taurine can neutralize hypochlorous acid, one of the reactive species generated by myeloperoxidase-halide system in neutrophils . In that reaction, taurine is converted to taurine chloramine, which is less toxic than hypochlorous acid and actually serves as a modulator of the immune system also by interfering with the production of several pro-inflammatory mediators and activation of the transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) . In addition, taurine has been proposed to directly activate peroxisome proliferator-activated receptor Î³ (PPARÎ³) in epithelial cells, a mechanism that may account for its protective action against inflammation-related diabetic retinopathy progression . In consideration of the involvement of chronic inflammation and NF-kB derived mediators in dystrophic muscle [87, 104, 105], the above immunomodulatory actions of taurine are of value.
In young rats on low-protein diets, depression of growth and food intake occur when additional tyrosine is given, which is followed by death at higher tyrosine intake levels. A unique effect of this amino acid is to induce corneal and paw lesions in rats fed low-protein diets with 3-5% tyrosine, but histopathological changes also occur in a variety of other tissues (1). These effects are moderated with time and higher levels of dietary protein or by limiting amino acids (1). The eye lesions were shown to consist of tyrosine crystals resulting from the high concentration and low solubility of tyrosine in tissue fluids (111,112). In addition, changes in catecholamine-mediated functions, e.g., blood pressure, were reported (113).
(1992 ) Normal development and behavior of mice lacking the neuronal cell-surface PrP protein . (2003 ) Deletion of N-terminal residues 23-88 from prion prion protein (PrP) abrogates the potential to rescue PrP-deficient mice from PrP-like protein/doppel-induced neurodegeneration . It has been reported that residues 23-29 of PrP can function as an autonomous â€œprotein transduction domainâ€ (PTD) that is capable of translocating polypeptides (either PrP itself or reporter proteins) across the lipid bilayer into the cytoplasm (Wadia et al., 2008).
However, some foods that are generally consumed possess innate toxins with potential harmful effect in human health. The current study looked at some of the toxins their chemical structures, their mechanism of toxicities, sources of the toxins and the effect of processing on the toxins with focus on saponin, glycosides, toxic protein/amino acids and polyphenols.
safely. The body is unable to store proteins or amino acids. There are several additional areas that researchers are interested in exploring regarding L-arginine and its effects on the human body. Although L-arginine is considered safe in moderate doses, too much L-arginine can have severe side effects, including death.
However, in general, there is little evidence of serious adverse effects in humans from most amino acid supplements. Nonetheless, for many amino acids, the data relevant to humans are very limited, so unanticipated adverse consequences of consuming large amounts cannot be ruled out.