Influence of goat colchicine specific antibodies on murine colchicine disposition

Colchicine antimitosis causes progression of S-(1,2-dichlorovinyl)-l-cysteine-induced injury leading to acute renal failure and death in mice

“…These results are consistent with Mirela et al (2000) who have shown that CLC treatment does not affect the expression of aquaporin 1 in rat straight and convoluted straight tubules. Ramano et al (2000) and Terrien et al (1989) reported decreased expression of aquaporin 1 after administration of two-to three-fold higher doses of CLC than used in our study. Our findings show that CLC at a dose of 2 mg/kg neither affects aquaporin 1 nor causes renal dysfunction.…”

Colchicine poisoning: report of a fatal case with body fluid and post-mortem tissue analysis by high-performance liquid chromatography

“…The results are not in agreement with those of Rochdi et al (1992), who found concentrations of 125 ng/g in the brain. However, high concentrations of colchicine were found in the liver, kidney and heart, as described also by Terrien et al (1989) in mice, and Rodchi et al (1992) in humans. Kintz et al (1997) reported colchicine level of 12 and 29 ng/mL in liver and heart, respectively, of a fatal case of colchicine poisoning.…”

PK/TD modeling for prediction of the effects of 8C2, an anti-topotecan mAb, on topotecan-induced toxicity in mice

“…High-affinity antibodies can drastically alter the time course of ligand exposure, and the rate and extent of these alterations depends on the pharmacokinetic properties of the antibody, the pharmacokinetics of the ligand, the binding kinetics between antibody and ligand, and the dosing protocols employed. In most cases, administration of high affinity antibodies leads to an increased binding of ligand in plasma, redistribution of ligand from tissues to the systemic circulation (Rosenblum et al, 1990), increased total plasma ligand concentrations, reduced ligand concentrations in tissues, and decreased unbound ligand concentrations in plasma (Balthasar and Fung, 1994; Pentel et al, 1991; Terrien et al, 1989; Valentine and Owens, 1996). However, antibodies often impart a “restrictive” effect on the clearance of the ligand, which often leads to increased total cumulative systemic exposure of the ligand (AUC) and increases in the half-life of ligand in plasma.…”