Effect of in vivo phenol or hydroquinone exposure on events related to neutrophil delivery during an inflammatory response

• Published in: Toxicology (Amsterdam) 2006-03, Vol.220 (2), p.126-135
• Main Authors: Macedo, S.M.D., Lourenço, E.L.B., Borelli, P., Fock, R.A., Ferreira, J.M., Farsky, S.H.P.
• Format: Article
• Language: English
• Subjects: Adhesion molecules; Animals; Biological and medical sciences; Delivery. Postpartum. Lactation; Glycogen - pharmacology; Gynecology. Andrology. Obstetrics; Hydroquinone; Hydroquinones - toxicity; Inflammation; Inflammation - chemically induced; Inflammation - immunology; Leukocyte Count; Leukocyte Rolling - drug effects; Leukocytes - drug effects; Leukocytes - immunology; Leukocyte–endothelial interaction; Male; Medical sciences; Mesentery - drug effects; Mesentery - physiology; Neutrophil Activation - drug effects; Neutrophil Infiltration - drug effects; Neutrophils - cytology; Neutrophils - drug effects; Neutrophils - immunology; Phenol; Phenol - toxicity; Rats; Rats, Wistar; Toxicology
• ISSN: 0300-483X; 1879-3185
• DOI: 10.1016/j.tox.2005.12.008

Phenol (PHE) and hydroquinone (HQ) are metabolites of benzene that affect leukocytes after solvent intoxication. Hence, we investigated the effects of PHE or HQ exposure on neutrophil mobilization during an inflammatory response. Male Wistar rats received intraperitoneal injections of PHE, HQ or vehicle only and assays were performed 24 h after the last dose. Quantifications of bone marrow or circulating leukocytes showed that only HQ exposure induced neutrophilia, probably due to the accelerated mobilization from the bone marrow compartment, since reduced numbers of segmented cells in the last phase of maturation were detected there. Intravital microscopy showed that circulating leukocytes of HQ-exposed rats increased their rolling behavior and adherence to the mesenteric postcapillary venule wall in vivo. The enhanced leukocyte–endothelium interaction was not dependent on microvascular reactivity or perivascular mast cell degranulation. Instead, it was the result of neutrophil activation, demonstrated by a decrease in l-selectin and an increase in β 2 integrin expression on neutrophil membranes. This pattern of neutrophil activation may have contributed to the higher number of neutrophils in the subcutaneous inflammatory response of HQ-exposed rats after oyster glycogen injection. Taken together, our results indicate that HQ exposure alters neutrophil mobilization, which results in an exacerbated response after an injury. Although PHE is endogenously metabolized to HQ, PHE exposure only induced an increment in rolling behavior, which was not sufficient to alter the inflammatory response.