Changes in renal function and oxidative damage in methamphetamine-treated rat

Tokunaga, Itsuo; Kubo, Shin‐ichi; Ishigami, Akiko; Gotohda, Takako; Kitamura, Osamu

doi:10.1016/j.legalmed.2005.07.003

Cited by 31 publications

(24 citation statements)

References 12 publications

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“…In both an acute and a chronic model of methamphetamine administration, immunohistochemical markers, renal function markers, and blood ion concentrations indicated cellular damage consistent with pathologic changes seen in autopsy samples from methamphetamine abusers (36,37). As can be seen in Figure 3, the kidney would have the highest exposure of all the organs to methamphetamine and its labeled metabolites, possibly accounting for the previously reported pathologic changes noted in autopsy samples from methamphetamine abusers.…”

Section: Discussionsupporting

confidence: 61%

PET Studies of d-Methamphetamine Pharmacokinetics in Primates: Comparison with l-Methamphetamine and ( )-Cocaine

Fowler

Kroll

Ferrieri

et al. 2007

Journal of Nuclear Medicine

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The methamphetamine molecule has a chiral center and exists as 2 enantiomers, d-methamphetamine (the more active enantiomer) and l-methamphetamine (the less active enantiomer). d-Methamphetamine is associated with more intense stimulant effects and higher abuse liability. The objective of this study was to measure the pharmacokinetics of d-methamphetamine for comparison with both l-methamphetamine and (2)-cocaine in the baboon brain and peripheral organs and to assess the saturability and pharmacologic specificity of binding. Methods: d-and l-methamphetamine and (2)-cocaine were labeled with 11 C via alkylation of the norprecursors with 11 C-methyl iodide using literature methods. Six different baboons were studied in 11 PET sessions at which 2 radiotracer injections were administered 2-3 h apart to determine the distribution and kinetics of 11 C-d-methamphetamine in brain and peripheral organs. Saturability and pharmacologic specificity were assessed using pretreatment with d-methamphetamine, methylphenidate, and tetrabenazine. 11 C-d-Methamphetamine pharmacokinetics were compared with 11 C-l-methamphetamine and 11 C-(2)-cocaine in both brain and peripheral organs in the same animal. Results: 11 C-d-and l-methamphetamine both showed high uptake and widespread distribution in the brain. Pharmacokinetics did not differ between enantiomers, and the cerebellum peaked earlier and cleared more quickly than the striatum for both. 11 C-d-Methamphetamine distribution volume ratio was not substantially affected by pretreatment with methamphetamine, methylphenidate, or tetrabenazine. Both enantiomers showed rapid, high uptake and clearance in the heart and lungs and slower uptake and clearance in the liver and kidneys. A comparison of 11 C-d-methamphetamine and 11 C-(2)-cocaine showed that 11 C-d-methamphetamine peaked later in the brain than did 11 C-(2)-cocaine and cleared more slowly. The 2 drugs showed similar behavior in all peripheral organs examined except the kidneys and pancreas, which showed higher uptake for 11 C-d-methamphetamine. Conclusion: Brain pharmacokinetics did not differ between d-and l-methamphetamine and thus cannot account for the more intense stimulant effects of d-methamphetamine. Lack of pharmacologic blockade by methamphetamine indicates that the PET image represents nonspecific binding, though the fact that methamphetamine is both a transporter substrate and an inhibitor may also play a role. A comparison of 11 C-d-methamphetamine and 11 C-(2)-cocaine in the same animal showed that the slower clearance of methamphetamine is likely to contribute to its previously reported longer-lasting stimulant effects relative to those of (2)-cocaine. High kidney uptake of d-methamphetamine or its labeled metabolites may account for the reported renal toxicity of d-methamphetamine in humans.

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Section: Discussionsupporting

confidence: 61%

PET Studies of d-Methamphetamine Pharmacokinetics in Primates: Comparison with l-Methamphetamine and ( )-Cocaine

Fowler

Kroll

Ferrieri

et al. 2007

Journal of Nuclear Medicine

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“…Oxidative stress is believed to play a crucial role in METH-induced toxicity in the brain and other tissues, as evidenced by findings in previous studies. However, a comparison of oxidative effects of METH in different organs has not been sufficiently studied previously [21, 58]. …”

Section: Discussionmentioning

confidence: 99%

“…The toxic effects of METH on the brain are well-known and are linked to oxidative stress; little information is available about the oxidative stress induced by METH in other organs. Tokunaga et al [21] studied changes in renal function and found that repeated METH administration induced oxidative DNA injury to the kidney, as a chronic or subacute influence.…”

Section: Introductionmentioning

confidence: 99%

Chlorogenic and Caftaric Acids in Liver Toxicity and Oxidative Stress Induced by Methamphetamine

Koriem

Soliman

2014

Journal of Toxicology

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Methamphetamine intoxication can cause acute hepatic failure. Chlorogenic and caftaric acids are the major dietary polyphenols present in various foods. The aim of this study was to evaluate the protective role of chlorogenic and caftaric acids in liver toxicity and oxidative stress induced by methamphetamine in rats. Thirty-two male albino rats were divided into 4 equal groups. Group 1, which was control group, was injected (i.p) with saline (1 mL/kg) twice a day over seven-day period. Groups 2, 3, and 4 were injected (i.p) with methamphetamine (10 mg/kg) twice a day over seven-day period, where groups 3 and 4 were injected (i.p) with 60 mg/kg chlorogenic acid and 40 mg/kg caftaric acid, respectively, one day before methamphetamine injections. Methamphetamine increased serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, bilirubin, cholesterol, low-density lipoprotein, and triglycerides. Also, malondialdehyde in serum, liver, and brain and plasma and liver nitric oxide levels were increased while methamphetamine induced a significant decrease in serum total protein, albumin, globulin, albumin/globulin ratio, brain serotonin, norepinephrine and dopamine, blood and liver superoxide dismutase, and glutathione peroxidase levels. Chlorogenic and caftaric acids prior to methamphetamine injections restored all the above parameters to normal values. In conclusion, chlorogenic and caftaric acids before methamphetamine injections prevented liver toxicity and oxidative stress where chlorogenic acid was more effective.

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“…Lipopolysaccharide [18], alcohol [19], methamphetamine [20], glycerol [21], and many other drugs can induce renal injury, including oxidative stress and inflammation in mice and rats. D-gal-treated mice have been often used in antioxidative pharmacology research.…”

Section: Discussionmentioning

confidence: 99%

Troxerutin protects the mouse kidney from d-galactose-caused injury through anti-inflammation and anti-oxidation

Fan

Zhang

Zheng

et al. 2009

International Immunopharmacology

121

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Changes in renal function and oxidative damage in methamphetamine-treated rat

Cited by 31 publications

References 12 publications

PET Studies of d-Methamphetamine Pharmacokinetics in Primates: Comparison with l-Methamphetamine and ( )-Cocaine

PET Studies of d-Methamphetamine Pharmacokinetics in Primates: Comparison with l-Methamphetamine and ( )-Cocaine

Chlorogenic and Caftaric Acids in Liver Toxicity and Oxidative Stress Induced by Methamphetamine

Troxerutin protects the mouse kidney from d-galactose-caused injury through anti-inflammation and anti-oxidation

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