Sentences with phrase «acts by reducing oxidative stress»

N - acetylcysteine acts by reducing oxidative stress and normalizing glutaminergic transmission.

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Stress resistance has not been assessed however and so the biological relevance of this finding is currently unknown.32 Several IER trials (75 - 85 % ER on restricted days) in overweight / obese populations have reported reductions in various markers of oxidative stress 37, 41, which in one study was accompanied by a complementary increase in the anti-oxidant uric acid.37 In a direct comparison of IER (75 % ER for two days / week) and CER, both ER strategies displayed equal efficacy in reducing levels of fast - acting advanced oxidation protein products (AOPP) after six months, which displayed a tendency to occur earlier (i.e. at three months) in the IER group.41 Levels of slow - acting (i.e. long term) AOPP tended to decrease in the IER group and increase in the CER group which the authors proposed may have resulted from IER - induced activation of autophagy, a key homeostatic cellular process in which dysfunctional or unnecessary cellular proteins are degraded and recycled.41 On the other hand, a follow - up study using similar IER / CER protocols demonstrated comparable reductions in AOPP in both groups after three months.48 Summary and Future Research DireStress resistance has not been assessed however and so the biological relevance of this finding is currently unknown.32 Several IER trials (75 - 85 % ER on restricted days) in overweight / obese populations have reported reductions in various markers of oxidative stress 37, 41, which in one study was accompanied by a complementary increase in the anti-oxidant uric acid.37 In a direct comparison of IER (75 % ER for two days / week) and CER, both ER strategies displayed equal efficacy in reducing levels of fast - acting advanced oxidation protein products (AOPP) after six months, which displayed a tendency to occur earlier (i.e. at three months) in the IER group.41 Levels of slow - acting (i.e. long term) AOPP tended to decrease in the IER group and increase in the CER group which the authors proposed may have resulted from IER - induced activation of autophagy, a key homeostatic cellular process in which dysfunctional or unnecessary cellular proteins are degraded and recycled.41 On the other hand, a follow - up study using similar IER / CER protocols demonstrated comparable reductions in AOPP in both groups after three months.48 Summary and Future Research Direstress 37, 41, which in one study was accompanied by a complementary increase in the anti-oxidant uric acid.37 In a direct comparison of IER (75 % ER for two days / week) and CER, both ER strategies displayed equal efficacy in reducing levels of fast - acting advanced oxidation protein products (AOPP) after six months, which displayed a tendency to occur earlier (i.e. at three months) in the IER group.41 Levels of slow - acting (i.e. long term) AOPP tended to decrease in the IER group and increase in the CER group which the authors proposed may have resulted from IER - induced activation of autophagy, a key homeostatic cellular process in which dysfunctional or unnecessary cellular proteins are degraded and recycled.41 On the other hand, a follow - up study using similar IER / CER protocols demonstrated comparable reductions in AOPP in both groups after three months.48 Summary and Future Research Directions
Ginger acts as a powerful antioxidant and has been shown to be effective in reducing oxidative stress caused by free radicals in the environment.
For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseases.
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