The effect of oxidative stress in myocardial cell injury in mice exposed to chronic intermittent hypoxia.
BACKGROUND
Obstructive sleep apnea syndrome (OSAS) is an important risk factor for cardiovascular diseases. Chronic intermittent hypoxia (CIH) is considered to be one of the most important causes of cardiovascular diseases in OSA patients. This repeated hypoxia and reoxygenation cycle is similar to hypoxia-reperfusion injury, which initiates oxidative stress. In this study, we observed cardiocytes injury induced by CIH and the effect of N-acetylcysteine (NAC).


METHODS
Thirty ICR mice were randomly assigned to 3 groups: control, CIH and NAC (CIH + NAC) groups. Malondialdehyde (MDA) and superoxide dismutase (SOD) of cardiocyte homogenates were measured. Serum lipids were measured by an instrument method. Serum cardiac troponin I (cTnI) was detected by enzyme-linked immunosorbent assays (ELISA). Myocardium pathological sections were observed.


RESULTS
(1) The SOD activity and MDA concentration of cardiocyte homogenates in the CIH group were significantly higher than in other groups (P < 0.005). The MDA concentration of the NAC group was lower than that of the control group (P < 0.01). (2) The serum cTnI concentration of the CIH and NAC groups was significantly higher than that of the control group (P < 0.01). (3) Serum triglyceride levels in the NAC group were lower than in the other groups (P < 0.01), while there were no significant differences in low density lipoprotein and high density lipoprotein among the three groups. (4) The degeneration of myocardium, transverse striation blurred, and fabric effusion were observed in tissue sections in the CIH and NAC groups. However, normal tissue was found in the control group.


CONCLUSIONS
The oxidative stress induced by CIH can injure cardiocytes and the injury effect can be partially inhibited by NAC.
Department of Respiratory Diseases, Jiangsu Geriatric Hospital, Nanjing, Jiangsu 210024, China.
Jian-nan
JN
Liu
Jie-xin
JX
Zhang
Gan
G
Lu
Yan
Y
Qiu
Di
D
Yang
Guo-yong
GY
Yin
Xi-long
XL
Zhang
D000111:Acetylcysteine / Q000494:pharmacology; D000818:Animals; D016166:Free Radical Scavengers / Q000494:pharmacology; D006321:Heart / Q000187:drug effects; D000860:Hypoxia / Q000503:physiopathology*; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008813:Mice, Inbred ICR; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology*; D011897:Random Allocation; D013482:Superoxide Dismutase / Q000378:metabolism
D016166:Free Radical Scavengers; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D000111:Acetylcysteine