Oup and steric aspects. The formation of a chelate complex decreases the reactivity Tonnes, the lower reactivity t of oxaliplatin, 7, 8 and 6 against explained Ren k Nnte. H the higher density of electrons leaving group, the less reactive complex: oxalate. The cellular Re accumulation As above for the compounds 2-5, the accumulation rate at the beginning increases with increasing lipophilicity increased Ht, suggesting that passive diffusion is the main mechanism of the beaches determination in the first minutes of incubation. The rate of the trailer Ufung of delay Struggled, the results of correlation analyzes indicated no significance of passive diffusion, either sensitive or resistant cell line. Reactive Ability to be an important factor in the influx via a mechanism independent Ngig lipophilicity. This is for oxaliplatin, 6 and 8 apply to the Erh increase the reactivity of these complexes leads to a t h higher accumulation rate at the beginning and end: 8 \ oxaliplatin \ 6 A Similar relationship was also found in studies with oxaliplatin, PtCl 2 and Pt 2. However, the R The exact exchange of the leaving group in the accumulation of platinum complexes is still unknown because we do not know what types of platinum are hit by the cell. Either the ligand exchange occurs formed in the cell culture Estrogen Receptor Pathway medium and reagents or complex chlorinated water, transported into the cell, or the exchange is responsible through direct interaction with proteins in the plasma membrane to the influx of platinum complexes. Making the flow by 50% for most compounds of the resistant cell line, a result of both reduced negative regulation of protein and Ver be Changes in the lipid composition of the membrane.
The more lipophilic analog of oxaliplatin, 7, requires further examination. Despite the low reactivity of t was cellular Re accumulation of 7 h and still relatively high Forth in the resistant cell line than in the sensitive cell line. Assess the influence of the structure of the ligand and the amine leaving group, we compared the cellular Re accumulation of 7 Similar to the reactive oxaliplatin and carboplatin and 6, react with the analog oxaliplatin and cisplatin. Interestingly, the concentration-time profiles of cisplatin and 6 Similar, suggesting a minor influence on the amine ligands. In this case, the reactivity of t to be crucial for the influx. However, the concentration profiles of carboplatin time and 7 were YOUR BIDDING different, although leaving the carrying of the same group. In this case, any au Ergew Similar high lipophilicity effect on the accumulation of 7 relative to the reactivity of t. This property makes The complex glicht apparently, to the resistance mechanism of the examined in a reduction of accumulation of other complexes leads to avoid. In our previous study of oxaliplatin analogues with different amine ligands, we observed a Similar behavior of the more lipophilic compound, 5 We have proposed that one Change in the biophysical properties of the plasma membrane of resistant cells, leading to a preferred transport of lipophilic complexes or through the membrane. This nnte k Explained Ren, the gr Ere Anh Ufung of 7 in the resistant cells than in sensitive counterparts. Comparison of the cellular show Ren accumulation of these complexes.
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