Progression of cyclophosphamide-induced acute renal metabolic damage in carnitine-depleted rat model

Abstract

Oxidative stress is not involved in CP-induced renal injury in this model. Carnitine deficiency and energy starvation constitute risk factors in and should be viewed as a mechanism during CP-induced nephrotoxicity. PLC prevents development of CP-induced nephrotoxicity by increasing intracellular carnitine content, intramitochondrial CoA-SH/acetyl-CoA ratio and energy production.

Urinary metabonomics elucidate the therapeutic mechanism of Orthosiphon stamineus in mouse crystal-induced kidney injury

“…Carnitine deficiency and energy starvation have been reported to play critical role in chemical-induced nephrotoxicity (Sayed-Ahmed, 2010). In contrast, acylcarnitines and particularly propionyl-L-carnitine, which is a product of the enzymatic esterification of carnitine (Murphy et al, 2012), have been described to prevent the development of renal failure by increasing intracellular carnitine levels and energy production (Sayed-Ahmed, 2010).…”

Acute Renal Endothelial Injury During Marrow Recovery in a Cohort of Combined Kidney and Bone Marrow Allografts

“…Drugs with potential nephrotoxicity were given to these patients before (cyclophosphamide) (32, 33) or after transplantation (cyclosporine or tacrolimus). CNIs cause renal failure by vascular toxicity, leading to vasoconstriction and tubular injury.…”

Protective effect of aminoguanidine against cyclophosphamide-induced oxidative stress and renal damage in rats

“…Intraperitoneal administration of CP has been reported to increase malondialdehyde (MDA), decrease in reduced glutathione (GSH), and decrease the activities of kidney's antioxidative enzymes, such as superoxide dismutase, glutathione peroxidase (GPx), glutathione reductase, and catalase. [7][8][9][10] There is growing evidence for the role of aminoguanidine (AG) as an antioxidant. Many studies have demonstrated that AG acts as an antioxidant, and prevents the loss of antioxidant enzyme activities as well as cellular damage.…”