• Title/Summary/Keyword: hepatic toxicity

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Hepatotoxic mechanism of diclofenac sodium on broiler chicken revealed by iTRAQ-based proteomics analysis

  • Sun, Chuanxi;Zhu, Tianyi;Zhu, Yuwei;Li, Bing;Zhang, Jiaming;Liu, Yixin;Juan, Changning;Yang, Shifa;Zhao, Zengcheng;Wan, Renzhong;Lin, Shuqian;Yin, Bin
    • Journal of Veterinary Science
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    • v.23 no.4
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    • pp.56.1-56.17
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    • 2022
  • Background: At the therapeutic doses, diclofenac sodium (DFS) has few toxic side effects on mammals. On the other hand, DFS exhibits potent toxicity against birds and the mechanisms remain ambiguous. Objectives: This paper was designed to probe the toxicity of DFS exposure on the hepatic proteome of broiler chickens. Methods: Twenty 30-day-old broiler chickens were randomized evenly into two groups (n = 10). DFS was administered orally at 10mg/kg body weight in group A, while the chickens in group B were perfused with saline as a control. Histopathological observations, serum biochemical examinations, and quantitative real-time polymerase chain reaction were performed to assess the liver injury induced by DFS. Proteomics analysis of the liver samples was conducted using isobaric tags for relative and absolute quantification (iTRAQ) technology. Results: Ultimately, 201 differentially expressed proteins (DEPs) were obtained, of which 47 were up regulated, and 154 were down regulated. The Gene Ontology classification and Kyoto Encyclopedia of Genes and Genomes pathway analysis were conducted to screen target DEPs associated with DFS hepatotoxicity. The regulatory relationships between DEPs and signaling pathways were embodied via a protein-protein interaction network. The results showed that the DEPs enriched in multiple pathways, which might be related to the hepatotoxicity of DFS, were "protein processing in endoplasmic reticulum," "retinol metabolism," and "glycine, serine, and threonine metabolism." Conclusions: The hepatotoxicity of DFS on broiler chickens might be achieved by inducing the apoptosis of hepatocytes and affecting the metabolism of retinol and purine. The present study could provide molecular insights into the hepatotoxicity of DFS on broiler chickens.

Hesperidin and Hesperetin Protect against Oxidative Stress on Hepatic Toxicity in Rats (Hesperidin과 Hesperetin의 간 손상 동물모델에서 산화적 스트레스에 대한 간 보호 효과)

  • Kim, Ji Hyun;Li, Li;Kim, Mi Suk;Cho, Eun Ju;Kim, Hyun Young;Choi, Jine Shang
    • Journal of Korean Medicine for Obesity Research
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    • v.22 no.1
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    • pp.1-10
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    • 2022
  • Objectives: To investigate the protective effect of hesperidin and hesperetin against oxidative stress in 2,2'-azobis (2-aminopropane) dihydrochloride (AAPH)-induced liver toxicity in rats. Methods: Hesperidin or hesperetin (200 mg/kg/day, respectively) was orally administered for 7 days once daily in rats. Subsequently, AAPH (50 mg/kg/day) was administered intraperitoneally. Lipid peroxidation, nitric oxide production, catalase activity, and protein expressions of nuclear factor-kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) in the liver tissues were measured. Results: Administration of hesperidin and hesperetin significantly decreased serum aspartate transaminase and alanine transaminase levels in AAPH-induced oxidative stress liver tissues compared with control group. Lipid peroxidation and nitric oxide (NO) production were also significantly reduced by hesperidin and hesperetin in AAPH-induced oxidative stress liver tissues. In particular, lipid peroxidation levels of hesperetin-administered group significantly decreased to 5.02 nmole/mg protein in oxidative stress rats. Hesperidin and hesperetin significantly increased antioxidant activity, such as that of catalase. Furthermore, administration of hesperidin and hesperetin substantially down-regulated the expression of NF-κB and iNOS in liver tissues. Administration of hesperidin reduced NO levels and iNOS expression more than in the hesperetin-administered group. Conclusions: Administration of hesperidin and hesperetin led to a reduction in AAPH-induced liver toxicity by regulating oxidative stress.

Effect of Water Extract in Fruits of Omija (Schizandra chinensis Baillon) on $CCI_4$ Toxicity ($CCl_4$ 독성에 미치는 오미자 열매의 물추출물의 효과)

  • Lee, Joung-Sook;Lee, Sung-Woo
    • Journal of the Korean Society of Food Culture
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    • v.5 no.2
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    • pp.253-257
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    • 1990
  • The effect of water extract in fruits of Omija (Schizandra chinensis Ballion) on liver function in expermental liver injuries induced by $CCl_4$. The levels of GPT, GOT activities in serum were decreased apparently on the dosage of water extract in fruits of Omija correspond to raw Omija 1g compared to control group. The levels of Microsomal protein, glycogen, and pyruvate in liver and of Urea nitrogen, GPT, GOT, LDH in serum showed a trend toward restoration of normalization. No effective of levels of hepatic G6P DH activity and serum free fatty acid by water extract in fruits of Omija.

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Hepatoprotective Activity of Bacopa monniera on D-galactosamine Induced Hepatotoxicity in Rats

  • Ramakrishnan, S.;Sumathi, T.
    • Natural Product Sciences
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    • v.13 no.3
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    • pp.195-198
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    • 2007
  • Hepatoprotective action of alcoholic extract of Bacopa monniera (BME) was evaluated on Dgalactosamine (D-GalN) induced rat liver toxicity. Bacopa monniera extract reduced the elevated serum enzyme activities of ALT, AST, ALP, LDH, ${\gamma}-GT$ and the formation of hepatic malondialdehyde induced by D-GalN. The alcholic extract of Bacopa monniera also significantly restored the decreased levels of glutathione and the decreased activities of glutathione peroxidase, glutathione reductase, superoxide dismutase, catalase and glucose-6-phosphatase. Therefore these results suggest that Bacopa monniera has hepatoprotective effect against D-GalN induced hepatotoxicity.

Effect of Spices on hepatic microsomal enzyme function in mice

  • Han, Yong-Bong;Shin, Kuk-Hyun;Woo, Won-Sick
    • Archives of Pharmacal Research
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    • v.7 no.1
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    • pp.53-56
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    • 1984
  • The effect of twenty two spices on liver microsomal monooxygense activity was tested as measured by alteration of hexobarbital (HB) narcosis and strychnine mortality in mice. Oral administration of seven spices for 7 consecutive days caused a significant shortening of the duration of HB-induced sleeping time. The treatment of mice with a single i. p. injection of 9 spices resulted in a significant prolongation of the sleeping time. White pepper, dill and fennel reduced the toxicity of strychnine. These results strongly indicated that some spices might affect the activity of liver microsomal drug metabolizing enzyme (DME) function.

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Acetaminophen Poisoning (아세트아미노펜 중독)

  • Chung, Sung-Pil;Kim, Seung-Ho;Lee, Hahn-Shick
    • Journal of The Korean Society of Clinical Toxicology
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    • v.6 no.1
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    • pp.1-8
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    • 2008
  • Acetaminophen (AAP) overdose can result in potentially serious hepatotoxicity. The ingested dose and time from ingestion to presentation are important prognostic factors. Toxic dose in adult is thought to be at least 10 g or 200 mg/kg. However, early management of acute overdose should be guided by the plasma AAP concentration. The antidote for AAP poisoning is N-acetylcysteine (NAC). It provides complete protection against hepatotoxicity if given within 8 h of acute overdose. If the concentration is above the possible toxicity line as predicted by the Rumack-Matthew nomogram, either the 72-hr oral or the 20-hr intravenous NAC regimen should be administered. NAC is also effective if started late in patients with established hepatic failure. This article summarizes the current consensus of clinical assessment and management for acute AAP overdose.

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Severe Acidosis after Massive Metformin Overdose (혈당 강하제 metformin 중독 후 발생한 심각한 산혈증 1례)

  • Kim, Bo-In;Jung, Jin-Hee;Eo, Eun-Kyung
    • Journal of The Korean Society of Clinical Toxicology
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    • v.6 no.1
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    • pp.42-44
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    • 2008
  • Metformin which is an oral hypoglycemic agents, acts by enhancing insulin sensitivity, decreasing hepatic glucose production and increasing peripheral utilization of glucose. Deliberate self poisoning with oral hypoglycemic agents is rare. The lactic acidosis associated with metformin toxicity is well described in the medical literature. Metformin overdose even in otherwise healthy patients may produce a profound and life threatening lactic acidosis. We report a case of massive metformin ingestion(75g) in a patient presenting with lactic acidosis and hypotension. She died 24h after presenting to our emergency department despite bicarbonate treatment and hemofiltration therapy.

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Two Cases of Acute Renal Failure Caused by Acute Paraquat Poisoning (급성 Paraquat 중독 후 발생한 급성 신부전 환자 2예)

  • 장통영;정용준;김관식;서관수;한명아;신선호;김동웅
    • The Journal of Korean Medicine
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    • v.21 no.4
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    • pp.276-285
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    • 2000
  • Paraquat is a very potent herbicide which causes fatal toxicity when ingested, and there is no specific antidote against it. Human ingestion induces acute renal failure, hepatic dysfunction and progressive respiratory failure with high mortality rate. Clinical investigation and medical treatment were done on two cases of acute renal failure caused by paraquat poisoning admitted to the Department of Internal Medicine, Wonkwang University Oriental Chonju Medical Hospital. We report two cases of patients who survived after acute paraquat intoxication, by means of oriental medicine such as Gamdutang, a typical antidote of toxins, chinese ink as an absorbent and burned powder of Rhei Radix et Rhizoma for laxative and so on, western medicine such as gastric lavage, diuretics and fluid therapy. We suggest more experiments and studies related to such treatment for paraquat poisoning be conducted.

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Effects of acute dibutyl phthalate administration on hepatic lipid peroxidation and gamma-glutamyl transferase activity in mice (마우스에서 dibutyl phthalate 급성 투여가 간 지질과산화와 gamma-glutamyl transferase 활성에 미치는 효과)

  • 최달웅;김영환
    • Journal of environmental and Sanitary engineering
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    • v.19 no.1
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    • pp.50-56
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    • 2004
  • Dibutyl phthalate (DBP) is used extensively in the plastic industry and has been known as an endocrine disruptor. Present study was undertaken to examine whether DBP can induce oxidative stress in mice. In this study, oxidative stress was measured in terms of the modification of lipid peroxidation and gamma-glutamyl transferase (GGT) activity. The serum toxicity index, level of lipid peroxidation and triglyceride (TG), and activity of GGT were measured in male ICR mice after a single administration of DBP (5 g/kg, po). DBP did not alter serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, glucose and cholesterol level. However, the treatment with DBP was found to significantly increase the level of lipid peroxidation in liver and lung. The TG content and activity of GGT in the liver of DBP-exposed animals was also increased. These results indicate that DBP can induce mild oxidative stress in mice. The GGT activity is considered to be increased as one of the adaptive defense mechanisms to oxidative stress induced by DBP.

Arsenite-induced Hepatotoxicity in Chang Liver and Clone 9 Cells

  • Yum, Young-Na;Ahn, Jin-Hong;Kim, Gi-Dae;Hwang, Myung-Sil;Kim, Sheen-Hee;Lim, Chul-Joo;Yang, Ki-Hwa;Kim, Dae-Kyung;Cho, Dae-Hyun
    • Proceedings of the Korean Society of Toxicology Conference
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    • 2003.05a
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    • pp.56-56
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    • 2003
  • The reactivity and toxicity of arsenic compounds depend on the their oxidative states. Exposure to arsenic causes many human health effects, including cardiovascular, hepatic and renal disease, in addition to cancer in kidney, liver, lung, urinary bladder and skin. The cytotoxic effects of arsenite on normal hepatocyte, which most of its biotranfomation takes place. (omitted)

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