To cite this article: Al-Said A. Haffor (2010) Effect of myrrh (Commiphoramolmol) on leukocyte levels before and during healing from gastric ulcer or skin injury, Journal of Immunotoxicology, 7:1, 68-75,

Myrrh, Commiphora molmol has been used as anti-inflammatory and wound healing commercial product. Leukocyte count had been reliable indicator for clinicians to monitor progress of healing for their patients. We hypothesized that myrrh supplement participate in the activation of leukocyte proliferation pathway prior and post skin injury and gastric ulcer. The purpose of the present study was to examine long-term effect of myrrh on leukocytes proliferation before injury and during different stages of healing. Results showed that all types of leukocytes were significantly (p < 0.05) higher in the myrrh-treated groups before and during healing. The pretreatment with myrrh offered a time-dependent rise in leukocytes proliferation. Microscopic examination of blood smear from myrrh-treated rats with skin injury, showed an elevated count of middle-sized lymphocytes and neutrophils that were characterized with well-defined nuclear lobules and rich-granules cytoplasm. Furthermore, the microscopic examinations of the spleen and lymph nodes of myrrh-treated rats with skin injury, showed an increased thickness of lymphatic sheath around the arterioles in the white pulp that was associated with high density of the medium-sized lymphocytes in the secondary lymphoid follicles in the lymph nodes with engorged sinusoids. As myrrh enhanced leukocytes proliferation before injury, it can be concluded that myrrh posse's antigenic-driven responses and that indicated some foreignness or toxicity of some constituents of myrrh. Because myrrh helped to maintain the relative rise of leukocytes counts throughout healing period and that implied it activated late steps of both proliferation and differentiation pathways for all types of leukocytes during effective phase of the specific immune responses.

Hyperoxia (HP) exposure inducts reactive oxygen species (ROS) in the lungs that may result in lung injury, including alveolar epithelial and endothelial cells. Lactate dehydrogenase (LDH) activity relates to glycolysis, whereas glutathione peroxidase (Gpx) activity relies on the pentose phosphate pathway (PPP). The purpose of this study was to examine early ROS-induced alveolar pathological changes in relation to the activity of glutathione peroxidase (GPx) and lactate dehydrogenase (LDH) activity. Twenty adult male rats, matched with age and body weight, were randomly assigned to two groups, control and experimental. The experimental group was exposed to hyperoxia for 24 h. Ultrastructure examination showed degenerated pneumocyte type I, containing swollen mitochondria associated with dilated rough endoplasmic reticulum, and was projecting into the alveolar lumen. Pneumocyte II showed mitochondria swelling and hyperplasia and was desquamated in structure, depleted in surfactant, and falling into the alveolar lumen. Pulmonary capillary showed distention without observed damage in the endothelial layer. Following HP, the average (+/-) free radical (FR) production increased significantly (p<.05) from the baseline control of 181.20+/-30.06 to 260.30+/-68.10 (Carr U) and average (+/-SD) GPx activity also increased significantly (p<.05) from the baseline control of 8178.30+/-2402.62 to 19,589.50+/-2392.44 (U/L), whereas average (+/-SD) LDH activity decreased significantly (p<.05) from baseline control of 194.11+/-75.52 to 42.68+/-11.41 (U/L), which demonstrated slowing down of glycolysis. Based on these results it can be concluded that exposure to high inspired oxygen inducted the buildup of mitochondria-driven ROS that was related to early injury in the alveolar epithelium without obvious endothelium injury.

The purpose of the present study was to examine the effects of periodic hyperoxia training (PHT) and/or continuous exposure to hyperoxia (HP) on free radical (FR) levels and biological antioxidant potentials (BAPs) in relation to ultrastructural pathological changes in myocytes. Thirty adult male rats were randomly assigned to three groups: control (C), HP, or PHT. HP rats were continuously subjected to atmospheres containing 100% O2 for 48 h, whereas PHT animals breathed 100% O2 for 30-min periods three times daily over a 3-week period. Ultrastructural examination of isolated myocytes from the HP rats showed that swelled mitochondria with constricted and proliferated cristae of the inner membrane were associated with disarrangement of myofibrils as well as the loss of I-banding. Heart tissue supernatant analyses also provided evidence of significantly higher FR levels in samples from the HP rats as compared with values noted with materials from control and PHT rats. In contrast, BAP was significantly higher in the samples from rats in the PHT group as compared levels associated with the control or the HP hosts. As HP resulted in mitochondrial pathological alterations in the cristae, this implied the induction of a myocardium oxidative stress (MOS). As PHT enhanced BAP, it may be concluded that PHT likely enhances an apparent antioxidant response that did not permit FR to build up. Because PHT elevations would be expected to help lower FR levels, it would seem that periodic hyperoxia training might induce an adaptive resistance in the heart against the formation of potentially toxicologically deleterious reactive metabolite species.

Hyperoxia has been widely used as model for oxidative stress. Free radicals (FR), suproxide anion (*O(-)(2)) and nitric oxide anion (*NO(-)), are highly toxic and have detrimental effects on nitroso-redox balance in the myocyte. Myocardium is rich with beta-adrenergic receptors and endothelial is the site of NO production. The authors hypothesized that graded doses of dobutamine result in hyperkinetic state, which shifts the nitroso-redox balance toward the buildup of reactive species in dose-dependent excess. The purpose of the present study was to investigate free radicals production and coronary endothelial cell pathological changes following increasing length of breathing oxygen (100% O(2)) and progressive doses of dobutamine. Thirty-five adult male rats, matched with age and body weight, were randomly assigned to 7 groups. The first group served as control (C) and the 2nd, 3rd, and 4th groups were exposed to hyperoxia (100% O(2) breathing) for 24,48, and 72 h, whereas the 5th, 6th, and 7th groups were injected dobutamine 10,20, and 30 microg kg(-1), respectively. Following the treatment condition for each group, animals were sacrificed and heart tissues were divided randomly into two parts. The first part was processed for the ultrastructure, using transmission electron microscope (TEM), and the second was homogenized for FR determination. TEM examination showed that O2 breathing for 24 h resulted in hypertrophy and proliferation of endothelial cells lining the coronary capillary, which was lodged by lymphoid cells. Distended and irregular contour of endothelium, enlarged nucleus, protrusion membrane, as well as pinocytotic vesicles were also observed. Free radicals (FR) production at all levels of hyperoxia exposures and dobutamine injections were significantly (p < .05) higher than control group. In addition, dobutamine induced higher relative FR production, as compared with hyperoxia, implying more severe myocyte injury. Based on the results of the present study, it can be concluded that O2 breathing for 24 h or higher resulted in variety of pathological changes of the endothelium of coronary capillary that were induced by the buildup of oxidants by-products. Because dobutamine caused relative higher in FR production levels, as compared with hyperoxia levels, throughout this implied it aggravated the myocyte capillaries' endothelium more heavily, which could have resulted in more intense ultrastructural deteriorations.