Hyperbaric oxygen treatment and N-acetylcysteine ameliorate acetaminophen-induced liver injury in a rat model.
An overdose of acetaminophen (APAP) produces centrilobular hepatocellular necrosis. We aimed to investigate the hepatoprotective effects of N-acetylcysteine (NAC) only and hyperbaric oxygen (O(2)) treatment (HBOT) combined with NAC, and their anti-inflammatory properties in liver tissue. In the current study, a total of 32 male Sprague Dawley rats were divided into 4 groups: sham, APAP, NAC, and NAC + HBOT. In the APAP, NAC, and NAC + HBOT groups, liver injury was induced by oral administration of 1 g/kg APAP. The NAC group received 100 mg/kg NAC per day. NAC + HBOT group received intraperitoneal injection of 100 mg/kg/day NAC and were given HBOT at 2.8 ATA pressure with 100% O(2) inhalation for 90 min every 12 h for 5 days. Rats in the sham group received distilled water only by gastric tube. All animals were killed on day 6 after APAP or distilled water administration. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, hepatic neopterin, tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6) levels were measured. There was a significant increase in serum AST and ALT activities in the APAP group compared with the sham group (in both p = 0.001). NAC and NAC + HBOT groups had significant decreases in hepatic neopterin, TNF-α, and IL-6 levels compared with the APAP group. APAP administration caused extensive hepatic necrosis. NAC and NAC + HBO treatments significantly reduced APAP-induced liver injury. Our results showed that the liver damage in APAP toxicity was attenuated by NAC and NAC + HBO treatments. NAC + HBOT exhibit hepatoprotective activity against APAP-induced liver injury in rats.
1Department of Biochemistry, Diskapi Yildirim Beyazit Training and Research Hospital, Diskapi, Ankara, Turkey.
M Y
MY
Taslipinar
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I
Aydin
U
U
Kaldirim
F N
FN
Aydin
M
M
Agilli
Y E
YE
Eyi
S K
SK
Tuncer
E
E
Altayli
F
F
Ucar
E
E
Macit
M
M
Toygar
N
N
Yigit
T
T
Cayci
D000082:Acetaminophen; D000111:Acetylcysteine / Q000494:pharmacology / Q000627:therapeutic use*; D018712:Analgesics, Non-Narcotic; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000473:pathology / Q000628:therapy*; D004195:Disease Models, Animal; D006931:Hyperbaric Oxygenation; D015850:Interleukin-6 / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D019798:Neopterin / Q000378:metabolism; D020011:Protective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D018712:Analgesics, Non-Narcotic; D000893:Anti-Inflammatory Agents; D015850:Interleukin-6; D020011:Protective Agents; D014409:Tumor Necrosis Factor-alpha; D000082:Acetaminophen; D019798:Neopterin; D000111:Acetylcysteine
Acetaminophen; N-acetylcysteine; hyperbaric oxygen; inflammation; liver injury