Triiodothyronine (T<sub>3</sub>) increases cisplatin nephrotoxicity in young and adult rats

Appenroth, Dorothea; Gambaryan, Stepan; Bakhteeva, V. T.; Winnefeld, K; Schröter, Heinz; Gerhardt, Steffen; Bräunlich, H

doi:10.1002/jat.2550100603

Cited by 3 publications

(1 citation statement)

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“…This is comparable with the investigations of Sukocheva and Carpenter [ 14 ] on mouse model of hepatotoxicity. One previous study had indicated that pretreatment with T3 enhanced CIS-induced nephrotoxicity in rats [ 37 ], the finding that was inversely demonstrated in the current work and that might be explained considering time invention. Exposure to gamma radiation was accepted to bring about dose-dependent loss of cell viability [ 38 ].…”

Section: Discussionsupporting

confidence: 54%

L-thyroxine modifies nephrotoxicity by regulating the apoptotic pathway: The possible role of CD38/ADP-ribosyl cyclase-mediated calcium mobilization

et al. 2017

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Thyroid hormones are well-established as a key regulator of many cellular metabolic pathways developed in various pathogeneses. Here, we dedicated the current work to investigate the role of thyroid hormone analogue (L-thyroxine, L-TH) in regulating the renal cytotoxicity using in vivo and in vitro models. Swiss mice were exposed to gamma radiation (IRR, 6Gy) or treated with cisplatin (CIS, 15 mg/kg, i.p.) for induction of nephrotoxicity. Remarkably, pretreatment with L-TH (1μg/kg) ameliorated the elevated kidney function biomarkers, oxidative stress and protected the renal tissue from the subsequent cellular damage. Likewise, L-TH inhibited the apoptotic cascade by down-regulating the extreme consumption of the cellular energy (ATP), the expression of caspase-3 and Bax, and the stimulation of cyclic ADP ribose (cADPR)/calcium mobilization. Moreover, incubation with L-TH (120nM/4h) significantly blocked the cytotoxicity of CIS on Vero cells and the depletion of NAD+ content as well as modified the ADP-ribose cyclase (CD38) enzymatic activity. High doses of L-TH (up to30 nM/4h) inversely increased the radiosensitivity of Vero cells towards IRR (up to 6Gy). On the other hand, L-TH did not interfere CIS-induced cytotoxicity of colorectal adenocarcinoma (Caco-2) cell line. In conclusion, pretreatment with L-TH could be a promising protective approach to the renal cellular damage induced during either CIS or IRR therapy by regulating the unbalanced oxidative status, the expression of pro-apoptotic biomarkers via modulation of cADPR mediated-calcium mobilization.

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Section: Discussionsupporting

confidence: 54%

L-thyroxine modifies nephrotoxicity by regulating the apoptotic pathway: The possible role of CD38/ADP-ribosyl cyclase-mediated calcium mobilization

et al. 2017

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Comparative Nephrotoxicity Studies of Cisplatin and its Iodinized Derivative in Rats

Appenroth

Kessler

Winnefeld

et al. 1991

Archives of Toxicology

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Role of Glutathione for Cisplatin Nephrotoxicity in Young and Adult Rats

Appenroth

Winnefeld

1993

Renal Failure

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Investigations were done in 10- and 55-day-old Wistar rats. Glutathione (GSH) level in kidney was decreased by 8 mmol buthionine sulfoximine (BSO)/100 g BW. There was no effect on the renal function and nephrotoxicity of cisplatin (0.6 mg CP/100 g BW) in adult rats. In young rats BSO treatment was followed by nephrotoxic effects. Pt concentration remained unaffected by BSO in young and adult rats. GSH concentration in kidney was increased by 100 mg acetyl-cysteine (accys)/100 g BW. CP nephrotoxicity was lower in young as well as in adult ac-cys-treated rats. Pt levels in renal tissue were significantly decreased in rats from both age groups. From our results we conclude that the beneficial effect of high GSH concentration in renal tissue on CP nephrotoxicity is the result of decreased Pt concentration in kidney.

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Triiodothyronine (T₃) increases cisplatin nephrotoxicity in young and adult rats

Cited by 3 publications

References 15 publications

L-thyroxine modifies nephrotoxicity by regulating the apoptotic pathway: The possible role of CD38/ADP-ribosyl cyclase-mediated calcium mobilization

L-thyroxine modifies nephrotoxicity by regulating the apoptotic pathway: The possible role of CD38/ADP-ribosyl cyclase-mediated calcium mobilization

Comparative Nephrotoxicity Studies of Cisplatin and its Iodinized Derivative in Rats

Role of Glutathione for Cisplatin Nephrotoxicity in Young and Adult Rats

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Triiodothyronine (T3) increases cisplatin nephrotoxicity in young and adult rats

Cited by 3 publications

References 15 publications

L-thyroxine modifies nephrotoxicity by regulating the apoptotic pathway: The possible role of CD38/ADP-ribosyl cyclase-mediated calcium mobilization

L-thyroxine modifies nephrotoxicity by regulating the apoptotic pathway: The possible role of CD38/ADP-ribosyl cyclase-mediated calcium mobilization

Comparative Nephrotoxicity Studies of Cisplatin and its Iodinized Derivative in Rats

Role of Glutathione for Cisplatin Nephrotoxicity in Young and Adult Rats

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Triiodothyronine (T₃) increases cisplatin nephrotoxicity in young and adult rats