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Effect of adenosine triphosphate on methylphenidate-induced oxidative and inflammatory kidney damage in rats
Bahtinur Yeter1, Zeynep Suleyman2, Seval Bulut3
1Department of Child Health and Diseases, Faculty of Health Sciences, Erzincan Binali Yildirim University, Erzincan, Türkiye.
Abstract:
The purpose of this trial was to assess the effects of methylphenidate on the kidney tissues and to investigate the protective effect of adenosine triphosphate (ATP) against possible methylphenidate nephrotoxicity in rats. The rats were separated into; healthy control (HG), methylphenidate (MPHG), ATP (ATPG), and ATP+ methylphenidate (AMPG). The ATPG and AMPG groups were administered ATP 4 mg/kg bw/d, and the HG and MPHG groups received distilled water intraperitoneally. One hour from, ATP and distilled water administration, methylphenidate 10 mg/kg bw/d was applied via oral gavage to the AMPG and MPHG groups once daily for 30 d (1 × 1). Animals were euthanized after 30 d and tissues were collected. The levels of certain oxidant/antioxidant parameters, pro-inflammatory cytokines, and Blood urea nitrogen (BUN) and creatinine levels were measured. Kidneys were also examined histopathologically. ATP inhibited the increase in oxidant and decrease antioxidant levels induced by methylphenidate. The amounts of pro-inflammatory cytokines were increased in methylphenidate-treated kidney tissue compared with the HG and AMPG groups. However, ATP increased oxidative damage markers and cytokines levels close to the healthy group. Serum BUN and creatinine levels increased with methylphenidate but ATP prevented BUN and creatinine from rising in the ATPG and MPHG groups. ATP also reduced the histopathological damage increased by methylphenidate. The potential efficacy of ATP in treating kidney damage induced by methylphenidate use.
Insights
Adenosine triphosphate (ATP) protects against methylphenidate-induced kidney damage in rats by reducing oxidative stress and inflammation. This study highlights ATP
Area of Science:
- Pharmacology and Toxicology
- Nephrology
- Biochemistry
Background:
- Methylphenidate is commonly prescribed but can have potential nephrotoxic effects.
- Oxidative stress and inflammation are key mechanisms in drug-induced kidney injury.
- Adenosine triphosphate (ATP) plays a crucial role in cellular energy metabolism and has shown protective properties.
Purpose of the Study:
- To evaluate the nephrotoxic effects of methylphenidate in a rat model.
- To investigate the potential protective role of adenosine triphosphate (ATP) against methylphenidate-induced kidney damage.
Main Methods:
- Rats were divided into four groups: control, methylphenidate, ATP, and ATP + methylphenidate.
- Animals were treated daily for 30 days with methylphenidate (10 mg/kg) or vehicle, and ATP (4 mg/kg) or vehicle.
- Kidney tissues were analyzed for oxidant/antioxidant parameters, pro-inflammatory cytokines, blood urea nitrogen (BUN), creatinine, and histopathological changes.
Main Results:
- Methylphenidate increased oxidative stress, pro-inflammatory cytokines, BUN, and creatinine levels, and caused histopathological damage.
- ATP administration significantly attenuated these methylphenidate-induced changes.
- ATP treatment normalized oxidant/antioxidant balance and reduced inflammatory markers and kidney damage.
Conclusions:
- Adenosine triphosphate (ATP) demonstrates significant protective effects against methylphenidate-induced nephrotoxicity in rats.
- ATP mitigates kidney damage by counteracting oxidative stress and inflammation.
- These findings suggest ATP's potential therapeutic utility in managing methylphenidate-associated kidney injury.
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