(GPx), and remove free radicals like peroxide, H 2 O 2 , superoxide, and nitric oxide
(Samarghandian et al. 2016). In diabetic rats, carvacrol reduced oxidative stress
through the improvement of the activity of antioxidant enzymes (Deng et al. 2013).
In vitro analysis showed that the amount of intracellular ROS production of mouse
V79 fibroblast cells depends on the dose-dependent manner of carvacrol. The production of ROS decreases with the increasing concentration of carvacrol (Ündeğer
et al. 2009a). Some anti-oxidant activities are also performed on in vivo studies.
Hydrogen peroxide resistance–induced damage to DNA in hepatic and testicular
tissue was gradually decreasing in rats when carvacrol was administered in drinking
water (at 30 and 60 mg/kg for 7 days or 15 and 30 mg/kg for 14 days) (Slamenova
et al. 2013). Other studies have also shown that carvacrol has a protective role
against lipid peroxidation and induces enhanced endogenous antioxidant defensive
mechanisms in hepatocellular carcinogenesis caused by N-nitrosodiethylamine and
antioxidant function against hepatotoxicity in rats. Carvacrol has enhanced the
reduced function of antioxidant enzymes and improved the lipid peroxidation in
ethanol-exposed rat hippocampus (Wang et al. 2017; Mehrjerdi et al. 2020).
13.9 Antimicrobial Effect
The efficacy of the carvacrol depends on their phenolic group as well as hydroxyl
group which is attached with the phenolic structure and increased membrane permeability by working on the micro-organism at low concentration. The inhibitory
activity of phenols may be clarified by associations with micro-organisms’ cell
membrane and is also associated with the compounds’ hydrophobicity. Most
hydrophobic molecules are usually harmful and the cytoplasmic membrane is often
the main source of harmful activity. Besides, lipophilic products showed a strong
affinity for cell membranes, and their insertions induced changes in the physicochemical properties of membranes and increased depletion of intercellular ATP
(Ultee et al. 2002; COX et al. 2007). The interactions between antimicrobial
compounds and cell membranes are defined to affect both the lipid order and the
stability of the bilayer, resulting in a decrease in membrane integrity and an increase
in the passive flux of protons through the membrane. This effect is documented
particularly for compounds with a log P greater than 3. By consensus, the most
effective antimicrobial compound was carvacrol, which has a log P of 3.52 (Ben
Arfa et al. 2006). Carvacrol, by partitioning the phospholipid fatty acid chains,
created ion channels across the membrane, eventually allowing ions to exit cytoplasm (Ultee et al. 2002). Carvacrol has showed bacteriostatic and bactericidal
activity on food pathogens such as Vibrio cholerae, Campylobacter jejuni, E. Coli,
Listeria monocytogenes, S. aureus, Staphylococcus epidermidis, Lactobacillus
sakei, P. aeruginosa, Pseudomonas putida, Streptococcus mutans, and Bacillus
subtilis (Friedman et al. 2002; Lambert et al. 2001; Mathela et al. n.d.;
Rattanachaikunsopon and Phumkhachorn 2010; Ravishankar et al. 2010). Also, the
presence of a free hydroxyl carvacrol group and its influence on the delocalized
13 Carvacrol (Origanum vulgare): Therapeutic Properties …
445
(Samarghandian et al. 2016). In diabetic rats, carvacrol reduced oxidative stress
through the improvement of the activity of antioxidant enzymes (Deng et al. 2013).
In vitro analysis showed that the amount of intracellular ROS production of mouse
V79 fibroblast cells depends on the dose-dependent manner of carvacrol. The production of ROS decreases with the increasing concentration of carvacrol (Ündeğer
et al. 2009a). Some anti-oxidant activities are also performed on in vivo studies.
Hydrogen peroxide resistance–induced damage to DNA in hepatic and testicular
tissue was gradually decreasing in rats when carvacrol was administered in drinking
water (at 30 and 60 mg/kg for 7 days or 15 and 30 mg/kg for 14 days) (Slamenova
et al. 2013). Other studies have also shown that carvacrol has a protective role
against lipid peroxidation and induces enhanced endogenous antioxidant defensive
mechanisms in hepatocellular carcinogenesis caused by N-nitrosodiethylamine and
antioxidant function against hepatotoxicity in rats. Carvacrol has enhanced the
reduced function of antioxidant enzymes and improved the lipid peroxidation in
ethanol-exposed rat hippocampus (Wang et al. 2017; Mehrjerdi et al. 2020).
13.9 Antimicrobial Effect
The efficacy of the carvacrol depends on their phenolic group as well as hydroxyl
group which is attached with the phenolic structure and increased membrane permeability by working on the micro-organism at low concentration. The inhibitory
activity of phenols may be clarified by associations with micro-organisms’ cell
membrane and is also associated with the compounds’ hydrophobicity. Most
hydrophobic molecules are usually harmful and the cytoplasmic membrane is often
the main source of harmful activity. Besides, lipophilic products showed a strong
affinity for cell membranes, and their insertions induced changes in the physicochemical properties of membranes and increased depletion of intercellular ATP
(Ultee et al. 2002; COX et al. 2007). The interactions between antimicrobial
compounds and cell membranes are defined to affect both the lipid order and the
stability of the bilayer, resulting in a decrease in membrane integrity and an increase
in the passive flux of protons through the membrane. This effect is documented
particularly for compounds with a log P greater than 3. By consensus, the most
effective antimicrobial compound was carvacrol, which has a log P of 3.52 (Ben
Arfa et al. 2006). Carvacrol, by partitioning the phospholipid fatty acid chains,
created ion channels across the membrane, eventually allowing ions to exit cytoplasm (Ultee et al. 2002). Carvacrol has showed bacteriostatic and bactericidal
activity on food pathogens such as Vibrio cholerae, Campylobacter jejuni, E. Coli,
Listeria monocytogenes, S. aureus, Staphylococcus epidermidis, Lactobacillus
sakei, P. aeruginosa, Pseudomonas putida, Streptococcus mutans, and Bacillus
subtilis (Friedman et al. 2002; Lambert et al. 2001; Mathela et al. n.d.;
Rattanachaikunsopon and Phumkhachorn 2010; Ravishankar et al. 2010). Also, the
presence of a free hydroxyl carvacrol group and its influence on the delocalized
13 Carvacrol (Origanum vulgare): Therapeutic Properties …
445