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Excess ROS can damage all major cellular constituents (DNA, proteins, and lipids) and even lead to cell death, apoptosis, hypertrophy, fibrosis, and contractile dysfunction in the myocardium [8, 11]

Recently, it was shown that recombinant human GSTs, in particular GSTP1, significantly contributed to the inactivation of AQ-derived QIs by catalyzing GSH-conjugation (Zhang et al., 2017a) ( Figure 1 )

While TA-65 administration did not affect the proportions of terminally differentiated CD8 + T-lymphocytes, it led to significant elevations in major lymphocyte subsets and a notable 62% reduction in high-sensitivity C-reactive protein (hsCRP) levels after 12 months compared to placebo

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