In the current study and others reports depolarization and increased permeability were demonstrated in eugenol-treated bacteria. The severity of GDC-0199 effect of eugenol on S. aureus biofilms results from the disruption of cell-to-cell connection, increased cell permeability causing leakage of internal cell contents to complete cell lysis, as seen in SEM analysis. Loss of membrane integrity and cell surface damage indicate that the bactericidal action of eugenol against S. aureus is elicited through the mechanism of membrane disruption and blocking of cell growth. Carvacrol is a phenolic monoterpenoid and a major constituent of oregano, which has been reported to disintegrate the outer membrane of bacteria. In current study, we detected a synergistic effect of eugenol with carvacrol against S. aureus biofilms. The MBEC was reduced _4-fold, suggesting a synergistic effect, as defined by the FICI_0.5. Both eugenol and carvacrol have been shown to disrupt the cell membrane and depolarize the cell. Moreover, carvacrol at low concentration forms channels through the membrane by pushing apart the fatty acid chains of the phospholipids and thereby allowing ions to leave the cytoplasm. Probably due to the structure differences, the two compounds interact in distinct ways with the cell membrane to enhance the biofilm eradication activity. Further study is warranted to determine the exact mechanism underlying the synergistic effect of these two compounds on S. aureus. The mechanisms of CCl4 toxicity are recognized. CCl4 is mainly activated by cytochrome P450 2E1 to form the trichloromethyl peroxy radical, which initiates lipid peroxidation by pulling out a hydrogen atom in the vicinity of a polyunsaturated fatty acid double bond. After propagation of the peroxidation process, lipids are finally degraded in small molecules such as malondialdehyde, a highly reactive aldehyde that can damage the plasma membranes. The end result inactivates calcium pump activity with calcium influx. All these alterations eventually lead to liver cell death accompanied by the release into the blood of intrahepatic enzymes. However, the mechanisms of CCl4-induced steatosis remain speculative. A close relationship between the hepatic sympathetic nerve supply and acute and chronic liver injury has previously been suggested. Some studies indicated that CCl4-induced acute hepatotoxicity was promoted by the systemic sympathetic tone or adrenoceptor stimulation, whereas other investigators found inconsistent effects of the sympathetic nervous system on the acute hepatotoxicity of CCl4. Thus the role of SNS action in CCl4 hepatotoxicity remains controversial and detailed mechanisms of SNS effect do not appear to have been sufficiently elucidated. Moreover, CCl4 is a well-known compound for the inducing immune responses and inflammation. Immune cells express various adrenergic and purinergic receptors that are sensitive to transmitters of the SNS. The production of cytokines/chemokines is modulated by activation of these receptors. We therefore hypothesized that the sympathetic activity has an effect on secretion of cytokines/chemokines in an animal with CCl4 intoxication. Here, we applied chemical sympathectomy to investigate the role of the SNS on acute toxic liver necrosis and steatosis induced by CCl4, and systemic pattern of pro- and anti-inflammatory FTY720 proteins in CCl4-poisoned mice. The role of SNS in CCl4-induced acute hepatotoxicity is still a matter of debate. It has been shown that selective sympathetic blockade confined to liver could alleviate liver injury by CCl4. Prior chemical sympathectomy with 6-OHDA abolished the CCl4 toxicity, suggesting that it is mediated through adrenergic stimulation of the liver, but the regulatory mechanism of sympathetic innervation remains poorly understood so far. However, it has been demonstrated that the inhibitory effect of noradrenaline on acute hepatotoxicity induced by CCl4. In addition, it has been reported that pretreatment of a ganglionic blocking agent diminished acute hepatotoxicity of CCl4 only in female Wistar rats rather than in males.