Albinism in plants - far beyond the loss of chlorophyll: Structural and physiological aspects of wild-type and albino royal poinciana (Delonix regia) seedlings.

The partial or complete loss of chlorophylls, or albinism, is a rare phenomenon in plants. In the present study, we provide the first report of the occurrence in albino Delonix regia seedlings and describe the morpho-physiological changes associated with albinism. Wild-type (WT) and albino seedlings were characterized. Leaflets samples were processed following common procedures for analysis with light, scanning and transmission electron microscopy. The chlorophyll a fluorescence parameters and the carbohydrate, lipid and soluble protein content were also determined in leaf and cotyledon samples of both albino and WT seedlings. Albino seedlings showed reduced growth. They also had lower chlorophyll and protein content in foliar tissues than WT seedlings, in addition to lower concentrations of lipids and carbohydrates stored in cotyledons. The chloroplasts of albino seedlings were poorly developed, with an undefined internal membrane system and the presence of plastoglobules. Wild-type seedlings had a uniseriate and hypoestomatic epidermis. The mesophyll was dorsiventral, consisting of a layer of palisade parenchyma and two to four layers of spongy parenchyma. In albino seedlings, the spongy parenchyma was compact, with few intercellular spaces, and the thickness of the mesophyll was larger, resulting in increased thickness of the leaf blade. Albino seedlings had higher stomatal density and number of pavement cells, although the stomata had smaller dimensions. In addition to the partial loss of chlorophylls, albino D. regia showed changes at physiological and structural levels, demonstrating the crucial nature of photosynthetic pigments during the development and differentiation of plant leaf tissues/cells.

CCR3 antagonist impairs estradiol-induced eosinophil migration to the uterus in ovariectomized mice

Eosinophils are abundant in the reproductive tract, contributing to the remodeling and successful implantation of the embryo. However, the mechanisms by which eosinophils migrate into the uterus and their relationship to edema are still not entirely clear, since there are a variety of chemotactic factors that can cause migration of these cells. Therefore, to evaluate the role of CCR3 in eosinophil migration, ovariectomized C57BL/6 mice were treated with CCR3 antagonist SB 328437 and 17β-estradiol. The hypothesis that the CCR3 receptor plays an important role in eosinophil migration to the mouse uterus was confirmed, because we observed reduction in eosinophil peroxidase activity in these antagonist-treated uteruses. The antagonist also influenced uterine hypertrophy, inhibiting edema formation. Finally, histological analysis of the orcein-stained uteruses showed that the antagonist reduced eosinophil migration together with edema. These data showed that the CCR3 receptor is an important target for studies that seek to clarify the functions of these cells in uterine physiology.

CCR3 antagonist impairs estradiol-induced eosinophil migration to the uterus in ovariectomized mice.

Eosinophils are abundant in the reproductive tract, contributing to the remodeling and successful implantation of the embryo. However, the mechanisms by which eosinophils migrate into the uterus and their relationship to edema are still not entirely clear, since there are a variety of chemotactic factors that can cause migration of these cells. Therefore, to evaluate the role of CCR3 in eosinophil migration, ovariectomized C57BL/6 mice were treated with CCR3 antagonist SB 328437 and 17ß-estradiol. The hypothesis that the CCR3 receptor plays an important role in eosinophil migration to the mouse uterus was confirmed, because we observed reduction in eosinophil peroxidase activity in these antagonist-treated uteruses. The antagonist also influenced uterine hypertrophy, inhibiting edema formation. Finally, histological analysis of the orcein-stained uteruses showed that the antagonist reduced eosinophil migration together with edema. These data showed that the CCR3 receptor is an important target for studies that seek to clarify the functions of these cells in uterine physiology.

Agonistic activity of tamoxifen, a selective estrogen-receptor modulator (SERM), on arthritic ovariectomized mice

Arthritis is positively associated with the decline of sex hormones, especially estrogen. Tamoxifen (TMX) is a selective estrogen receptor modulator, possessing agonist or antagonistic activity in different tissues. Thus, the objective of this study was to investigate the effect of TMX on the zymosan-induced arthritis model. Female Swiss normal and ovariectomized (OVX) mice were divided into groups and treated for five days with TMX (0.3, 0.9 or 2.7 mg/kg) or 17-β-estradiol (E2, 50 µg/kg). On the fifth day, arthritis was induced and 4 h later, leukocyte migration into joint cavities was evaluated. The neutrophil migration in OVX animals, but not in normal mice, treated with TMX (all tested doses) was significantly decreased compared with mice that received the vehicle (P≤0.05). Similarly, this effect was also demonstrated in the E2-treated group. Therefore, the present study demonstrates that TMX presented agonist effects in inhibiting neutrophil migration and preventing arthritis progression in OVX mice.

Agonistic activity of tamoxifen, a selective estrogen-receptor modulator (SERM), on arthritic ovariectomized mice.

Arthritis is positively associated with the decline of sex hormones, especially estrogen. Tamoxifen (TMX) is a selective estrogen receptor modulator, possessing agonist or antagonistic activity in different tissues. Thus, the objective of this study was to investigate the effect of TMX on the zymosan-induced arthritis model. Female Swiss normal and ovariectomized (OVX) mice were divided into groups and treated for five days with TMX (0.3, 0.9 or 2.7 mg/kg) or 17-ß-estradiol (E2, 50 µg/kg). On the fifth day, arthritis was induced and 4 h later, leukocyte migration into joint cavities was evaluated. The neutrophil migration in OVX animals, but not in normal mice, treated with TMX (all tested doses) was significantly decreased compared with mice that received the vehicle (P≤0.05). Similarly, this effect was also demonstrated in the E2-treated group. Therefore, the present study demonstrates that TMX presented agonist effects in inhibiting neutrophil migration and preventing arthritis progression in OVX mice.