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Acrolein, a Highly Toxic Aldehyde Generated Under Oxidative Stress in Vivo, Aggravates the Mouse Liver Damage After Acetaminophen Overdose

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Acrolein, a Highly Toxic Aldehyde Generated Under Oxidative Stress in Vivo, Aggravates the Mouse Liver Damage After Acetaminophen Overdose Biomedical Research (Tokyo) 35 (6) 389-395, 2014 Acrolein, a highly toxic aldehyde generated under oxidative stress in vivo, aggravates the mouse liver damage after acetaminophen overdose 1 1 2 1 1 Tomoya ARAI *, Ryo KOYAMA *, Makoto YUASA , Daisuke KITAMURA , and Ryushin MIZUTA 1 Research Institute for Biomedical Sciences, 2 Department of Pure and Applied Chemistry, Faculty of Science and Technology, Tokyo University of Science, 2669 Yamazaki, Noda, Chiba 278-0022, Japan (Received 17 September 2014; and accepted 3 October 2014) ABSTRACT Although acetaminophen-induced liver injury in mice has been extensively studied as a model of human acute drug-induced hepatitis, the mechanism of liver injury remains unclear. Liver injury is believed to be initiated by metabolic conversion of acetaminophen to the highly reactive interme- diate N-acetyl p-benzoquinoneimine, and is aggravated by subsequent oxidative stress via reactive oxygen species (ROS), including hydrogen peroxide (H2O2) and the hydroxyl radical (•OH). In this study, we found that a highly toxic unsaturated aldehyde acrolein, a byproduct of oxidative stress, has a major role in acetaminophen-induced liver injury. Acetaminophen administration in mice resulted in liver damage and increased acrolein-protein adduct formation. However, both of them were decreased by treatment with N-acetyl-L-cysteine (NAC) or sodium 2-mercaptoethane- sulfonate (MESNA), two known acrolein scavengers. The specificity of NAC and MESNA was confirmed in cell culture, because acrolein toxicity, but not 2H O2 or •OH toxicity, was inhibited by NAC and MESNA. These results suggest that acrolein may be more strongly correlated with acet- aminophen-induced liver injury than ROS, and that acrolein produced by acetaminophen-induced oxidative stress can spread from dying cells at the primary injury site, causing damage to the ad- jacent cells and aggravating liver injury. Acetaminophen-induced liver injury in mice has conversion to the reactive intermediate N-acetyl p- been used as a model of human acute drug-induced benzoquinoneimine (NAPQI) by cytochrome P-450 hepatitis and an in vivo model of necrosis (5, 6). (14). NAPQI covalently binds essential hepatocellu- Acetaminophen is a widely prescribed analgesic lar proteins, and is eliminated by glutathione. As the drug, and is also sold in numerous preparations as a primary endogenous non-protein sulfhydryl, gluta- single compound or in combination with other med- thione is a major scavenger of free radicals. High ications. Although it is generally safe, an overdose doses of acetaminophen deplete glutathione, thereby of acetaminophen can cause severe liver failure with increasing the formation of reactive oxygen species significant mortality. Despite substantial efforts in (ROS), such as hydrogen peroxide (H2O2) and the the past, the mechanism of acetaminophen-induced hydroxyl radical (•OH). ROS and NAPQI are free liver injury remains unclear. Acetaminophen-induced to bind critical cellular proteins, which may result in liver injury is thought to be initiated by its metabolic the reduction of antioxidant enzymes, enhancement of lipid peroxidation, and induction of hepatic ne- crosis (14). Address correspondence to: Dr. Ryushin Mizuta, Re- search Institute for Biomedical Sciences, Tokyo Univer- Acrolein (CH2=CHCHO), a highly reactive α, sity of Science, 2669 Yamazaki, Noda, Chiba 278-0022, β-unsaturated aldehyde, is a common pollutant found Japan Tel: +81-4-7121-4072, Fax: +81-4-7121-4079 E-mail: [email protected] *These authors contributed equally to this work. 390 T. Arai et al. in the environment. Notably, endogenous acrolein is the Tokyo University of Science. generated during oxidative stress (10). Acrolein can be formed in various tissues via lipid peroxidation Acetaminophen-induced liver necrosis. Mice were (19), polyamine oxidation (16) and via metabolism fasted 14 ~ 16 h before acetaminophen injection but of drugs, such as the anticancer drug cyclophospha- were allowed access to water. Acetaminophen was mide (7). Acrolein is primarily metabolized via rap- suspended in 50% Mili-Q water and 50% propylene id reaction with the sulfhydryl groups of glutathione. glycol and was intraperitoneally (ip) injected into Thus, acrolein contributes directly to cellular oxida- mice (600 mg/kg body weight). NAC (1000 mg/kg) tive stress via loss of glutathione (7). Acrolein can and MESNA (1000 mg/kg) were injected ip immedi- form Michael-type addition adducts with cellular ately after acetaminophen injection. Mice were sacri- components, particularly proteins and DNA, result- ficed at 12 h after acetaminophen injection to collect ing in cell toxicity. Elevated levels of acrolein and serum and tissues. Serum alanine aminotransferase acrolein-adducts have been found in ex vivo biologi- (ALT) levels were determined with an automated cal samples from patients, including the plasma of analyzer (Hitachi 7140; Hitachi Instruments Service patients with renal failure (13) and the brains of pa- Co., Tokyo, Japan). A piece of the liver from each tients with neurologic disorders (21). Acrolein can mouse was fixed with formalin and embedded in easily move across cell membranes and tissues due paraffin for hematoxylin-eosin (H&E) staining or to its solubility in water and alcohol; thus, high con- immunohistochemistry. Other pieces of the liver centrations of acrolein produced by lipid peroxida- were frozen in liquid nitrogen and were stocked in a tion or polyamine oxidation can spread from dying −80°C freezer. cells at the primary site of injury, resulting in dam- age and/or death in adjacent cells (10). Extraction of total RNA and reverse transcription Sodium 2-mercaptoethanesulfonate (MESNA), a polymerase chain reaction. Total RNA was extract- thiol compound, has been shown to scavenge acrole- ed from the removed liver tissues using TRIzol in both experimentally and clinically. MESNA inter- (Sigma-Aldrich, St. Louis, USA) according to the acts with acrolein and forms an inactivate compound, manufacturer’s instructions. Ten micrograms of total which is detectable using mass spectrometry (18). RNA were reverse-transcribed into cDNA using Su- As mentioned before, acrolein is metabolized from perscript with oligo (dT) primer (Invitrogen, Carls- the anticancer drug cyclophosphamide, and is known bad, USA). For examining the expression of heme to cause hemorrhagic cystitis. To prevent this side oxigenase-1 (Ho-1) gene and glyceraldehyde 3-phos- effect during cancer chemotherapy, MESNA has phate dehydrogenase (Gapdh) gene, quantitative been routinely given to patients, and has successive- polymerase chain reaction (q-PCR) was conducted ly decreased the incidence of hemorrhagic cystitis using THUNDERBIRD SYBR qPCR Mix (Toyobo, (18). Another thiol compound N-acetyl-L-cysteine Osaka, Japan) and the following primers according (NAC) is known as a glutathione pro-drug that is to the manufacturer’s instructions. Ho-1 Forward: approved for clinical use and is routinely used to 5’-TGGGTCCTCACTCTCAGCTT-3’, Ho-1 Reverse: treat acetaminophen-induced liver injury (11). Re- 5’-GTCGTGGTCAGAACATGG-3’, Gapdh Forward: cently, it was also shown that NAC directly inter- 5’-GGAGAAACCTGCCAAGTATGA-3’, Gapdh Re- acts with acrolein and forms an inactive compounds verse: 5’-CCCTGTTGCTGTAGCCGTATT-3’. (22). Here we show that acrolein-adducts are produced Histopathology. Excised liver was fixed in 10% for- in the livers of acetaminophen-treated mice, and that malin and embedded in paraffin. Four micron serial MESNA and NAC ameliorate acetaminophen-mediat- sections were used for H&E and TdT-mediated ed liver injury by neutralizing acrolein toxicity, which dUTP Nick-End Labeling (TUNEL) staining. For suggests that acrolein plays a critical role in the the TUNEL assay, the DeadEnd Fluorometric pathogenesis of acetaminophen-induced liver injury. TUNEL System (Promega, Madison, USA) was used according to the manufacturer’s protocol. For immunohistochemical analysis to detect acrolein, MATERIAL AND METHODS deparaffinized sections were immersed in 0.3% 2H O2 Animal treatment. C57BL/6 mice were purchased in methanol to eliminate endogenous peroxidase ac- from Sankyo-Lab Service (Tsukuba, Japan). All ex- tivity, followed by rinsing with a phosphate buffered perimental procedures using mice were approved by saline (PBS). Acrolein readily reacts with lysine res- the Institutional Animal Care and Use Committee at idues of proteins to form Nε-(3-formyl-3,4-de- Acrolein-induced liver damage 391 hydropiperidino)lysine (FDP-lysine) (19). Sections NAC that is a glutathione pro-drug and is routinely were then incubated with mouse anti-FDP-lysine an- used to treat acetaminophen-induced liver injury tibody (NOF CORPORATION, Tokyo, Japan) and, (11). Histopathological analysis was conducted to following rinsing with PBS, sections were incubated directly examine hepatic injury (Fig. 1A–D). H&E with peroxidase-conjugated anti-mouse immuno- staining of acetaminophen-treated liver sections re- globulin (Histofine Simple Stain Mouse stain kit) vealed hepatocyte necrosis in the area surrounding (Nichirei Co., Tokyo, Japan). Peroxidase activity on the central veins (Fig. 1B, top, arrows). DNA dam- the sections was developed with 3,3’-diaminobenzi- age in the liver sections was assessed by TUNEL. dine tetrahydrochloride (Nichirei Co.) as the sub- The TUNEL assay was initially developed to deter- strate and then the sections were counterstained with mine apoptosis, but recently we reported that even metyleneblue. The samples were
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