Protective effects of exogenous β-hydroxybutyrate on paraquat toxicity in rat kidney

Teng, Wei; Tian, Wei; Liu, Fangning; Xie, Guanghong

doi:10.1016/j.bbrc.2014.04.074

Cited by 52 publications

(40 citation statements)

References 34 publications

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“…TNF-α is an inflammatory marker and known macrophagic cytokine (43,44). Also, previous studies have shown that paraquat-induced renal toxicity is caused by oxidative stress and inflammation, and ROS plays a role in this toxicity (25). Our findings shown that paraquat increased the serum and renal TNF-α gene expression; which is consistent with previous study (3).…”

Section: Discussionsupporting

confidence: 92%

“…MDA is considered as a lipid peroxidation biomarker (38). In the present study, paraquat administration led to increase both the serum and renal MDA and serum protein carbonyl levels by producing oxidant agents which is consist with previous studies (25,29,35). Silymarin administration, however, has reduced serum PC and serum and renal MDA levels (Figure 2), which could be an indication of silymarin effects on inhibiting the oxidation of proteins and lipids, which is consistent with previous results (9,39).…”

Section: Discussionsupporting

confidence: 91%

“…Paraquat is secreted by proximal tubules before renal damage, but tubular damages happen with an increase in paraquat concentration. In paraquat-induced renal toxicity, primarily the glomerular coatings (podocytes) are damaged; then, tubular degeneration, and the formation of eosinophilic granular cytoplasm is happen in distal and proximal tubules (25)(26)(27).…”

Section: Discussionmentioning

confidence: 99%

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Protective and anti-inflammatory effects of silymarin on paraquat-induced nephrotoxicity in rats

Sharifi-Rigi¹,

Heidarian²

2019

J Herbmed Pharmacol

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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Protective and anti-inflammatory effects of silymarin on paraquat-induced nephrotoxicity in rats

Sharifi-Rigi¹,

Heidarian²

2019

J Herbmed Pharmacol

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“…SOD and CAT have essential role in the body against oxidative stress (Manoharan & Prabu, 2014;Sikander et al, 2013). Superoxide dismutase has a key role to eliminate the toxic effects of superoxide anion (Han et al, 2014;Wei, Tian, Liu, & Xie, 2014). Also, catalase converts H 2 O 2 to oxygen and water in protecting cells against hydrogen peroxide (Han et al, 2014;Sharifinasab, Banaee, Mohiseni, & Noori, 2016).…”

Section: Discussionmentioning

confidence: 99%

Ameliorative effects ofN‐acetyl cysteine on diclofenac‐induced renal injury in male rats based on serum biochemical parameters, oxidative biomarkers, and histopathological study

Nouri

Heidarian

2019

J Food Biochem

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Diclofenac (DIC) can cause nephrotoxicity in humans. In this study, we evaluated the protective effects of N‐acetyl cysteine (NAC) on DIC‐induced nephrotoxicity. Rats were assigned to four groups. Group 1 was control group; group 2 administrated with DIC only; group 3 administrated with DIC plus NAC and group 4 was treated with DIC and silymarin. Then, the oxidative biomarkers in serum and kidney were evaluated. In group 2, DIC caused a remarkable elevation (p < 0.05) in the levels of serum uric acid, TNF‐α, creatinine, urea, GOT, and GPT, protein carbonyl, malondialdehyde (MDA), and renal TNF‐α gene expression, relative to control group. In treated groups with NAC and silymarin, a noticeable reduction (p < 0.05) was seen in mentioned levels of biochemical parameters. NAC showed that it could reduce the abnormality of biochemical parameters and histopathological changes which is induced by DIC. Practical applications N‐acetyl cysteine (NAC) has a potential to ameliorate renal histopathological changes and improving renal activity of antioxidant enzymes in nephrotoxicity by diclofenac. Also, NAC has a potential to reduce inflammatory gene expression in the diclofenac‐induced nephrotoxicity. Additionally, NAC can be considered as an antioxidant which reduces renal MDA and serum protein carbonyl due to nephrotoxicity by diclofenac.

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“…In our previous study, we observed a significant positive trend in the rate of ESRD associated with increasing lifetime use of paraquat among pesticide applicators (Lebov et al, 2015). Exposure to paraquat produces reactive oxygen species (ROS) and related oxidative stress in renal cells (Wei et al, 2014), which can lead to renal cell apoptosis and necrosis (Kashihara et al, 2003); therefore, one possible biological mechanism for the association with paraquat, and other ROS-generating pesticides, is through repeated exposures over the lifetime, causing slow incremental renal cell damage and eventual renal dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Pesticide exposure and end-stage renal disease risk among wives of pesticide applicators in the Agricultural Health Study

Lebov

Engel

Richardson

et al. 2015

Environmental Research

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Background Pesticide exposure has been found to cause renal damage and dysfunction in experimental studies, but epidemiological research on the renal effects of chronic low-level pesticide exposure is limited. We investigated the relationships between end-stage renal disease (ESRD) among wives of licensed pesticide applicators (N = 31,142) in the Agricultural Health Study (AHS) and (1) personal pesticide use, (2) exposure to the husband's pesticide use, and (3) other pesticide-associated farming and household activities. Methods AHS participants reported pesticide exposure via self-administered questionnaires at enrollment (1993–1997). ESRD cases were identified via linkage to the United States Renal Data System. Associations between ESRD and pesticide exposures were estimated with Cox proportional hazard regression models controlling for age at enrollment. Models of associations with farming and household factors were additionally adjusted for personal use of pesticides. Results We identified 98 ESRD cases diagnosed between enrollment and 31 December 2011. Although women who ever applied pesticides (56% of cohort) were less likely than those who did not apply to develop ESRD (Hazard Ratio (HR): 0.42; 95% CI: 0.28, 0.64), among women who did apply pesticides, the rate of ESRD was significantly elevated among those who reported the highest (vs. lowest) cumulative general pesticide use (HR: 4.22; 95% CI: 1.26, 14.20). Among wives who never applied pesticides, ESRD was associated with husbands' ever use of paraquat (HR = 1.99; 95% CI: 1.14, 3.47) and butylate (HR = 1.71; 95% CI: 1.00, 2.95), with a positive exposure–response pattern for husband’s cumulative use of these pesticides. Conclusions ESRD may be associated with direct and/or indirect exposure to pesticides among farm women. Future studies should evaluate indirect exposure risk among other rural populations.

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Protective effects of exogenous β-hydroxybutyrate on paraquat toxicity in rat kidney

Cited by 52 publications

References 34 publications

Protective and anti-inflammatory effects of silymarin on paraquat-induced nephrotoxicity in rats

Protective and anti-inflammatory effects of silymarin on paraquat-induced nephrotoxicity in rats

Ameliorative effects ofN‐acetyl cysteine on diclofenac‐induced renal injury in male rats based on serum biochemical parameters, oxidative biomarkers, and histopathological study

Pesticide exposure and end-stage renal disease risk among wives of pesticide applicators in the Agricultural Health Study

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