The reduction of NOx urinary excretion and the high concentration of nitrotyrosine in the rats plasma and organs exhibited that an interaction between nitric oxide (NO) and ROS could contribute to the pathogenesis of hypertension in BSO-treated rats (Eiserich et al., 1995)
However, the authors noted that the results were heterogeneous, and except for LDL-cholesterol, the results, while statistically significant, were not clinically significant.21 A 2016 study found that in patients with elevated LDL, triglyceride, and lipoprotein (a) levels who received 2 g of L-carnitine plus 20 mg/day of simvastatin had a statistically significant but modest reduction in lipoprotein (a) compared with patients who received the simvastatin plus placebo.22 A meta-analysis of 17 clinical trials that included 1,625 adults with chronic heart failure found that supplementing with 1 to 6 g/day of L-carnitine for seven days to three years improved clinical symptoms and cardiac function compared with conventional treatment, and the benefits did not vary by supplement dose or study duration.23 A 2022 systemic review and dose-response meta-analysis of 22 randomized controlled human trials found that L-carnitine supplementation did not have a significant effect on blood pressure.24 A 2022 study that used Mendelian randomization found that genetically predicted higher endogenous L-carnitine levels were nominally associated with higher risk of CAD and heart failure in men and women, although the association did not hold for CAD in women from some data sources
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But previous studies have hypothesized oxidative stress as a common biochemical signature 26 and even shown some evidence in circulating serum redox proteins (e.g., myeloperoxidase) 59, 75 among LC patients
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Uric acid (UA), historically primarily linked to gout, has garnered increasing attention in the realm of neurodegenerative diseases due to its potential neuroprotective properties and emerging roles in mitigating oxidative stress and neuroinflammation [6]
