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1 Introduction Busulfan, a bifunctional DNA-alkylating agent, is widely applied as a chemotherapeutic in combination with cyclophosphamide, cytarabine, and fludarabine before allogeneic hematopoietic cell transplantation (HCT) ( The clinical application of busulfan is complicated by its high inter- and intra-individual pharmacokinetics/pharmacodynamics (PK/PD) variability, particularly in children ( Furthermore, owing to its narrow therapeutic index and large PK/PD variability, administering an initial busulfan IV dose based only on body weight (WT) may result in failure to reach the target therapeutic window ( Model-informed precision dosing utilizes population PK (popPK) models combined with maximum posterior Bayesian estimation to optimize both initial and subsequent dosing regimens based on TDM measurements ( GST alpha 1 ( GSTA1 ) genetic variations, and dosing schedule (day/time) are the most well-documented factors contributing to busulfan clearance variability ( Body size descriptors, including body surface area (BSA), fat-free mass (FFM), and normal fat mass (NFM), significantly influence busulfan PK in pediatric patients ( mat ), and distribution volume (V) based on FFM ( Time-varying CL was observed over a 4-day treatment with an every-6-h dosing regimen of busulfan ( Genetic polymorphisms in GSTA1 are associated with 8%27% reduction in CL ( Given this intricate interplay of physiological and pharmacological factors, comprehensive understanding of busulfan PK characteristics becomes essential for target exposure attainment
Thus, NO ultimately acts as an antioxidant by shunting superoxide to peroxynitrite to nitrate
In a crossover study by Vrieling et al., lycopene was observed to increase the concentrations of circulating insulin-like growth factor binding proteins (IGFBP)-1 and 2, thereby reducing the binding of IGF-I to its receptor, which may indirectly result in decreased bioavailability of IGF-I, potentially playing a preventive role in the development of colorectal cancer (Vrieling et al., 2007) (Figure 3)
Exclusion of sulfide:quinone oxidoreductase from mitochondria causes Leigh-like disease in mice by impairing sulfide metabolism
7 8 9 10 In these cases chronic oxidative stress can be generated, leaving existing anti-oxidant defenses overwhelmed
