Glutathione S-transferases T1 null genotype is associated with susceptibility to aristolochic acid nephropathy

Chen, Bicheng; Bai, Yongheng; Sun, Mei; Ni, Xin; Yang, Yunxiu; Yang, Yumei; Zheng, Shimin; Xu, Fei; Dai, Shengchuan

doi:10.1007/s11255-011-0082-z

Cited by 14 publications

(14 citation statements)

References 28 publications

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“…And the associations between common genotypes of CYP1A1, NQO1 (NAD (P)H quinone oxidoreductase 1), MDR1 (P-glycoprotein) and glutathione S-transferase (GST) and AAN risk were investigated. Results found that only GST null genotype was related to AAN susceptibility (Chen et al, 2012). In this study, we find that AAI is a substrate of BCRP.…”

Section: Discussionsupporting

confidence: 53%

“…The interaction between AAI and intestinal efflux drug transporters has not been investigated yet. Chen et al reported that there was no relationship between MDR1 polymorphism and AAN risk (Chen et al, 2012), which could not prove whether AAI was a substrate of MDR1.…”

Section: Discussionmentioning

confidence: 97%

“…Difference may be caused by the complex condition in vivo and in combination with other factors. Previous research indicated that AAN was not developed in all patients exposed to AA (Chen et al, 2012). Researchers speculated that gene polymorphism might determine the susceptibility to AAN.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Aristolochic acid I is a substrate of BCRP but not P-glycoprotein or MRP2

Qin

Shen

et al. 2015

Journal of Ethnopharmacology

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 97%

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Aristolochic acid I is a substrate of BCRP but not P-glycoprotein or MRP2

Qin

Shen

et al. 2015

Journal of Ethnopharmacology

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“…These genetic variations appear to be important determinants of cancer risk or other toxic effects of many xenobiotics (Stiborová et al 2008a , b , 2009 ). The combination of polymorphic enzymes along with environmental exposure to AA may result in an increased risk for the development of BEN/AAN (Atanasova et al 2005 ; Toncheva et al 2004 ; Toncheva 2006 ; Chen et al 2012a ). Hence, research over the last two decades has aimed to identify the enzymes principally involved AA metabolism (reviewed in Stiborová et al 2008a , b , 2009 , 2013b , 2014a , c , 2015b ).…”

Section: Metabolism Of Aristolochic Acidmentioning

confidence: 99%

Balkan endemic nephropathy: an update on its aetiology

2016

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Balkan endemic nephropathy (BEN) is a unique, chronic renal disease frequently associated with upper urothelial cancer (UUC). It only affects residents of specific farming villages located along tributaries of the Danube River in Bosnia-Herzegovina, Croatia, Macedonia, Serbia, Bulgaria, and Romania where it is estimated that ~100,000 individuals are at risk of BEN, while ~25,000 have the disease. This review summarises current findings on the aetiology of BEN. Over the last 50 years, several hypotheses on the cause of BEN have been formulated, including mycotoxins, heavy metals, viruses, and trace-element insufficiencies. However, recent molecular epidemiological studies provide a strong case that chronic dietary exposure to aristolochic acid (AA) a principal component of Aristolochia clematitis which grows as a weed in the wheat fields of the endemic regions is the cause of BEN and associated UUC. One of the still enigmatic features of BEN that need to be resolved is why the prevalence of BEN is only 3–7 %. This suggests that individual genetic susceptibilities to AA exist in humans. In fact dietary ingestion of AA along with individual genetic susceptibility provides a scenario that plausibly can explain all the peculiarities of BEN such as geographical distribution and high risk of urothelial cancer. For the countries harbouring BEN implementing public health measures to avoid AA exposure is of the utmost importance because this seems to be the best way to eradicate this once mysterious disease to which the residents of BEN villages have been completely and utterly at mercy for so long.

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“…However, not all individuals exposed to AA are susceptible to develop AAN. Chen 15 suggested that glutathione s-transferases T1 null genotype is associated with susceptibility to aristolochic acid nephropathy.…”

Section: Discussionmentioning

confidence: 99%

Acute kidney injury induced by aristolochic acid in patients with primary glomerular nephritis

et al. 2013

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Results: In the AAN-CGN group, six patients complained with gastrointestinal symptoms, such as nausea, vomiting, or loss of appetite. The rest of seven cases were asymptomatic or minimally uncomfortable, who were found with elevated serum creatinine (Scr) in the follow up of CGN. Compared with the control group, the patients in AAN-CGN group had higher levels of serum uric acid, urine n-acetyl-b-D-glucosaminidase, and urine protein excretion (366.2 AE 122.8 vs. 218.0 AE 125.8 mmol/L, p ¼ 0.037; 9.74 AE 4.4 vs. 1.38 AE 1.01 g/d, p ¼ 0.001; 61.2 AE 21.9 vs. 27.4 AE 15.8 m/g Á cr, p ¼ 0.007, respectively). In addition to, the AAN-CGN patients had an absolutely prominent percentage of macromolecule substance in the urine protein electrophoresis (25.0 AE 6.32 vs. 15.8 AE 7.8%, p ¼ 0.029). The occurrence of hypokalemia and excretion of aminoaciduria were lower than that in the control group. Pathologically, 84.6% of patients were found with tubular brush border dropping, 30.8% with naked tubular basement membrane, and 15.4% with different stages of vascular lesion. There were no statistical differences in the above-mentioned pathological parameters between the two groups. In the follow-up, 10 patients with AAN-CGN recovered with normal Scr, accounting for 76.9%, which was better than the recovery in the control group. Conclusion: Patients with acute AAN-CGN manifested with a great mass of urine protein excretion, low incidence of hypokalemia and aminoaciduria, however, the tubular-interstitial lesions were similar to the isolated AAN.

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Glutathione S-transferases T1 null genotype is associated with susceptibility to aristolochic acid nephropathy

Abstract: This study supports the hypothesis that polymorphisms related to drug metabolism such as GSTT1 may be an important factor influencing the development of AAN in the Chinese Han population exposed to AA.

Cited by 14 publications

References 28 publications

Aristolochic acid I is a substrate of BCRP but not P-glycoprotein or MRP2

Aristolochic acid I is a substrate of BCRP but not P-glycoprotein or MRP2

Balkan endemic nephropathy: an update on its aetiology

Acute kidney injury induced by aristolochic acid in patients with primary glomerular nephritis

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