Magnesium protects against cisplatin-induced acute kidney injury by regulating platinum accumulation.
نویسندگان
چکیده
Despite its success as a potent antineoplastic agent, ∼25% of patients receiving cisplatin experience acute kidney injury (AKI) and must discontinue therapy. Impaired magnesium homeostasis has been linked to cisplatin-mediated AKI, and because magnesium deficiency is widespread, we examined the effect of magnesium deficiency and replacement on cisplatin-induced AKI in physiologically relevant older female mice. Magnesium deficiency significantly increased cisplatin-associated weight loss and markers of renal damage (plasma blood urea nitrogen and creatinine), histological changes, inflammation, and renal cell apoptosis and modulated signaling pathways (e.g., ERK1/2, p53, and STAT3). Conversely, these damaging effects were reversed by magnesium. Magnesium deficiency alone significantly induced basal and cisplatin-mediated oxidative stress, whereas magnesium replacement attenuated these effects. Similar results were observed using cisplatin-treated LLC-PK1 renal epithelial cells exposed to various magnesium concentrations. Magnesium deficiency significantly amplified renal platinum accumulation, whereas magnesium replacement blocked the augmented platinum accumulation after magnesium deficiency. Increased renal platinum accumulation during magnesium deficiency was accompanied by reduced renal efflux transporter expression, which was reversed by magnesium replacement. These findings demonstrate the role of magnesium in regulating cisplatin-induced AKI by enhancing oxidative stress and thus promoting cisplatin-mediated damage. Additional in vitro experiments using ovarian, breast, and lung cancer cell lines showed that magnesium supplementation did not compromise cisplatin's chemotherapeutic efficacy. Finally, because no consistently successful therapy to prevent or treat cisplatin-mediated AKI is available for humans, these results support developing more conservative magnesium replacement guidelines for reducing cisplatin-induced AKI in cancer patients at risk for magnesium deficiency.
منابع مشابه
CALL FOR PAPERS Novel Therapeutics in Renal Diseases Magnesium protects against cisplatin-induced acute kidney injury by regulating platinum accumulation
Malvika H. Solanki, Prodyot K. Chatterjee, Madhu Gupta, Xiangying Xue, Andrei Plagov, Margot H. Metz, Rachel Mintz, Pravin C. Singhal, and Christine N. Metz Elmezzi Graduate School of Molecular Medicine, Manhasset, New York; The Center for Immunology and Inflammation, Feinstein Institute for Medical Research, North Shore-LIJ Health System, Manhasset, New York; and Hofstra North ShoreLIJ School ...
متن کاملMagnesium protects against cisplatin-induced acute kidney injury without compromising cisplatin-mediated killing of an ovarian tumor xenograft in mice.
Cisplatin, a commonly used chemotherapeutic for ovarian and other cancers, leads to hypomagnesemia in most patients and causes acute kidney injury (AKI) in 25-30% of patients. Previously, we showed that magnesium deficiency worsens cisplatin-induced AKI and magnesium replacement during cisplatin treatment protects against cisplatin-mediated AKI in non-tumor-bearing mice (Solanki MH, Chatterjee ...
متن کاملLipocalin2 Protects Human Embryonic Kidney Cells against Cisplatin–Induced Genotoxicity
Cisplatin is one of the most useful chemotherapeutics which performs its cytotoxic effectvia accumulation of platinum resulting in oxidative stress, and destruction of cell DNA. Thiscould probably cause secondary cancers in healthy tissues. Lipocalin2 (Lcn2) is a protein whichits expression is increased in oxidative stresses. Therefore, the present study was performedto evaluate the protective ...
متن کاملLipocalin2 Protects Human Embryonic Kidney Cells against Cisplatin–Induced Genotoxicity
Cisplatin is one of the most useful chemotherapeutics which performs its cytotoxic effectvia accumulation of platinum resulting in oxidative stress, and destruction of cell DNA. Thiscould probably cause secondary cancers in healthy tissues. Lipocalin2 (Lcn2) is a protein whichits expression is increased in oxidative stresses. Therefore, the present study was performedto evaluate the protective ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- American journal of physiology. Renal physiology
دوره 307 4 شماره
صفحات -
تاریخ انتشار 2014