Fig. 4.

Inflammatory markers in ethanol (EtOH)-fed rats following fracture and treatment with n-acetyl cysteine (NAC). (A) Serum TNF-α levels were increased in response to EtOH compared to controls (p < 0.0001). NAC significantly (NS) reduced these levels in the EtOH-fed rats, with a significant (p < 0.02) interaction to diet. (B) Fracture callus tissue TNF-α levels in the EtOH-fed animals was approximately 5 times that of control animals (p < 0.0001), which was reduced significantly (**p < 0.001) by NAC treatment, with an interaction to diet (p < 0.001). (C) Serum IFN-γ levels were higher in the EtOH-fed rats compared to controls (p < 0.0001). These levels were significantly (***p < 0.005) reduced to near control levels by NAC treatment with a significant (p < 0.005) interaction with diet. (D) Fracture callus tissue IFN-γ levels increased 3 times more in the EtOH-fed rats compared to controls (NS), and NAC treatment reduced it to control levels (NS). There was a significant (p < 0.05) interaction. (E) Serum IL-6 levels were increased in the serum of EtOH fed compared to controls (p < 0.01) and NAC treatment of EtOH-fed animals restored IL-6 almost to control level (*p < 0.02). (F) Fracture callus tissue IL-6 levels in the tissue callus were increased over control-fed animals and decreased in the EtOH fed with NAC, yet significance was not reached between the groups. (G) Serum IL-2 levels were not affected by EtOH feeding or NAC treatment. However, there was a significant (p < 0.04) interaction with diet. (H) Fracture callus tissue IL-2 level in the callus was more than 2-fold from controls, which was restored to control level (*p < 0.03) by NAC treatment of EtOH-fed animals, with a significant (p < 0.02) interaction with diet. N = 4 animals per group.