Since the ground-breaking study numerous studies have been carried out to clarify the role of hemethiolate monooxygenases in detoxification of PAH in the intestine. These studies have been related to identification and allocation of different PAH-metabolizing CYPs, to transcriptional and translational control of their expression and to regulation of their activity by xenobiotics from industrial processes or dietary intake. Today, it is clear that CYP1A1 is the key enzyme in metabolizing PAH, while CYP1A2 predominantly converts polar carcinogenic amines. The intestinal expression of murine CYP1A1 is considered to be minimal under non-stimulated conditions and might depend on flavonoid content in the chow. As observed previously, CYP1A2 expression was constitutively higher in the liver compared to that in the intestine, but remained unchanged after BaP feeding, Mildronate though a compensatory CYP1A2 induction in cyp1a12/2 mice was reported previously. Already under non-stimulated conditions, a significant suppression of CYP1A1 mRNA expression was measured in TLR22/2 mice in the current study. In contrast to that, this difference was not noted at the protein level, which might be explained by an increased protein stability phenomenon. The results from the intervention part of the study, in which both types of genotypes were fed BaP, which is a strong inducer of CYP1, confirmed our working hypothesis that the AHR-ARNT system regulating intestinal CYP1A expression depends virtually on intact TLR2 signaling. In line with previous findings, the initially low expression of both mRNA and protein of CYP1A1 in the murine intestine can considerably be increased by BaP feeding in animals with a functional TLR2 receptor. This induction of hydroxylase activity results in induction of both metabolic activation and detoxication of PAH. Metabolic activation, generating reactive intermediates capable of binding to DNA, was considered for decades to be the key pro-carcinogenic process. This concept seemed substantiated by studies on mice with high levels of active CYP1A1, which were more susceptible to cancers and genotoxicity when the PAH was brought in direct contact with the corresponding organs, but not after oral, systemic application. However, BaP feeding results in much higher acute toxicity, lethality, and formation of BaP-DNA adducts in the gastrointestinal tract, liver, and other organs of CYP1A12/2 mice. Hence, in the intact animal, intestinal CYP1A1 activity seems important in elimination and detoxification of PAH and is, in all likelihood, an important Echinatin factor in cancer prevention, especially when the activity of phase II enzymes is taken into consideration. The assumption that a high activity of CYPs in the gastrointestinal tract is protective in cancer development is also substantiated by a study in which significantly suppressed levels of three CYPs were found in non-malignant intestinal tissue of patients with adenoma compared to healthy controls. Based on the findings of the current study, the protection of inner organs from the effects of BaP feeding by intestinal CYP1A1 depends on the functional activation of the TLR2 receptor and, therefore, on the presence of an intestinal microflora providing ligands for TLR2. Hypertrophic scarring generally occurs following surgery, trauma and especially burns, which is a common proliferative disorder of dermal fibroblasts and results from an overproduction of collagen and excessive deposition of extracellular matrix. Nevertheless the good preventive effect of a drug does not mean its favorable therapeutic action.