Serum biochemical and histopathological changes related to the hepatic function in pigs following atrazine treatment

Gojmerac, Tihomira; B, Kartal; Žurić, Marijan; Ćurić, Stipica; Mitak, Mario

doi:10.1002/jat.2550150315

Cited by 24 publications

(16 citation statements)

References 16 publications

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“…Liver is an essential organ involved in the metabolism of exogenous toxic substance and also a primary target of ATR toxicity. It is known to cause hepatic damage in frogs, fish, birds, pigs, and rodents . The use of histologic and ultrastructural analysis allowed for the damage of target organelle in the microsomes by exposure to ATR .…”

Section: Discussionmentioning

confidence: 99%

Activating nuclear xenobiotic receptors and triggering ER stress and hepatic cytochromes P450 systems in quails (Coturnix C. coturnix) during atrazine exposure

Qin

Lin

et al. 2017

Environmental Toxicology

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Atrazine (ATR) is one of the most widely detected contaminant in the ecosystem. Nuclear xenobiotic receptors are activated by herbicides and induce the transcription of CYP450 isoforms involved in xenobiotic metabolism and transport. However, little is known about hepatic nuclear xenobiotic receptors in birds are responsible for ATR-induced hepatotoxicity via regulating the cytochrome P450 enzyme systems (CYP450s). The objective of this study was to investigate the mechanism of ATR hepatotoxicity in quails. For this purpose, male quails were dosed by oral gavage from sexual immaturity to maturity with 0, 50, 250, and 500 mg/kg/day ATR for 45 days. The results showed that ATR exposure caused the hepatotoxicity damage and endoplasmic reticulum (ER) degeneration. It suggested that ER is a target organelle of ATR toxicity in hepatocytes. ATR exposure disrupted the hepatic CYP450s homeostasis. This study also demonstrated that ATR triggered the CYP450 isoforms transcription via activating the hepatic CAR/PXR pathway. The present study provides new insights regarding the mechanism of the ATR-induced hepatotoxicity through activating nuclear xenobiotic receptors and triggering ER stress and hepatic CYP450s in quails.

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Section: Discussionmentioning

confidence: 99%

Activating nuclear xenobiotic receptors and triggering ER stress and hepatic cytochromes P450 systems in quails (Coturnix C. coturnix) during atrazine exposure

Qin

Lin

et al. 2017

Environmental Toxicology

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“…Liver is viewed as a primary organ for atrazine metabolism, which is known to cause hepatic damage in mammalian [15, 43, 44]. However, whether the effects of atrazine have the potential influence to the cardiac and hepatic function of birds still remain unclear.…”

Section: Discussionmentioning

confidence: 99%

A novel mechanism underlies atrazine toxicity in quails (Coturnix Coturnix coturnix): triggering ionic disorder via disruption of ATPases

Lin

Qin

et al. 2016

Oncotarget

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The widely used atrazine has been reported to exhibit extensive ecological hazards. Due to the biological accumulation, atrazine elicits widespread toxic effects on different organisms. However, true proof for the mechanism of atrazine-induced toxicity is lacking. To determine the potential mechanism by which atrazine exerted toxic effects, quails were treated with atrazine (0, 50, 250 and 500 mg/kg) by gavage administration for 45 days. Atrazine significantly increased the histological alterations and serum creatine kinase, lactate dehydrogenase and choline esterase levels. A marked disorder in ionic (Na+, K+, Ca2+ and Mg2+)contents and the decrease of ATPases (Na+-K+-ATPase, Ca2+-ATPase, Mg2+-ATPase and Ca2+-Mg2+-ATPase) activities were observed in the heart and liver of atrazine-exposed quails. Of note, it was also observed that atrazine suppressed the transcription of Na+, K+ transfer associated genes (Na+-K+-ATPase subunits) and Ca2+ transfer associated genes (Ca2+-ATPase subunits, solute carriers) in heart and liver. In conclusion, atrazine induced cardiac and hepatic damage via causing the ionic disorder, triggering the transcription of the ion transporters and leading the histopathological and functional alternations in the heart and liver of quails. This study demonstrated atrazine significantly induced the ionic disorder via decreasing the ATPases activities and disturbing the transcription of the ion transporters.

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“…[12] It is known to cause hepatic damage in rats and pigs;[131415] disrupt the functioning of the reproductive tissues;[161718] cause DNA damage and genotoxicity in the stomach, kidney, and liver of rats;[1920] damage rat erythrocytes[21] as well as induce oxidative stress in several experimental models. [8212223] We previously reported that ATZ at a dose of 120 mg/kg induces oxidative stress in rat tissues and blood at 16 days of treatment, and that the oxidative stress was associated with increased lipid peroxidation and changes in the antioxidative system.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of quercetin on atrazine-induced oxidative stress in the Liver, Kidney, Brain, and Heart of adult wistar rats

Abarikwu¹

2014

Toxicol Int

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Background:The conflicting roles of quercetin against tissue pathologies associated with oxidative stress are known.Objective:To evaluate the effect of quercetin at doses of 5 mg/kg (Q5) or 10 mg/kg (Q10) against atrazine (120 mg/kg, ATZ)-induced oxidative stress in various tissues of rats.Materials and Methods:Adult male albino Wistar rats were administered ATZ, Q5, and Q10 alone or in combination for 16 days. At the end of the 16th day, the animals were sacrificed by cervical dislocation; and the blood, heart, brain, kidney and liver were collected and used for biochemical determinations and histopathological examination.Results:Q10 but not Q5 attenuated ATZ-induced increase in the levels of serum enzyme markers sorbitol dehydrogenase (SDH), acid phosphatase (ACP), alkaline phosphatase (ALP), and aspartate aminotransferase (AST). The heart was less susceptible to ATZ-induced oxidative stress than the liver, kidney, and brain of treated animals, and there were tendencies for synergistic effects in the heart and liver of Q5 + ATZ-treated rats. Oxidative stress-induced by ATZ in terms of increased lipid peroxidation level and superoxide dismutase (SOD) activity was decreased in the brain of the Q5 + ATZ-treated rats but not that of the Q10 + ATZ-treated rats. Conversely, histopathological changes and oxidative stress-induced by ATZ in terms of elevated lipid peroxidation level, decreased SOD, and catalase (CAT) activities were prevented in the kidney and liver of the Q10 + ATZ-treated rats but not that of the Q5 + ATZ-treated rats.Conclusion:Quercetin at the investigated doses and especially the low dose may not protect against ATZ-induced oxidative stress in rat tissues in an overall sense.

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Serum biochemical and histopathological changes related to the hepatic function in pigs following atrazine treatment

Cited by 24 publications

References 16 publications

Activating nuclear xenobiotic receptors and triggering ER stress and hepatic cytochromes P450 systems in quails (Coturnix C. coturnix) during atrazine exposure

Activating nuclear xenobiotic receptors and triggering ER stress and hepatic cytochromes P450 systems in quails (Coturnix C. coturnix) during atrazine exposure

A novel mechanism underlies atrazine toxicity in quails (Coturnix Coturnix coturnix): triggering ionic disorder via disruption of ATPases

Protective effect of quercetin on atrazine-induced oxidative stress in the Liver, Kidney, Brain, and Heart of adult wistar rats

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