Perfil proteico de tilápia nilótica chitralada (Oreochromis niloticus), submetida ao estresse crônico por hipóxia / Proteic electrophoretic profile of chitralada tilapia nilotic (Oreochromis niloticus), exposed to hypoxia chronic stress

Avaliou-se a variação da resposta secundária ao estresse causado por hipóxia durante 18 dias, em sistema de recirculação, em uma linhagem de tilápia nilótica (Oreochromis niloticus), chitralada, refletida no perfil proteico eletroforético do peixe e avaliou-se a diferença entre sexos para essa resposta. Foram utilizados 126 peixes, sendo 60 machos e 66 fêmeas, ambos com média de peso de 800g. O estresse crônico por hipóxia alterou (P<0,05) os valores médios relativos de albumina, α+β-globulinas e de γ-globulina, provocou alteração (P<0,05) nos níveis de proteína total relativo ao aumento no grupo dos machos, diminuição significativa dos valores médios absolutos de albumina devido à diminuição nas fêmeas e à diminuição de γ-globulina nos machos. As variantes proteicas, albumina e γ-globulina tiveram influência do sexo.

This study evaluated the secundary response variation to hypoxia stress in a strain of chitralada nilotic tilapia (Oreochromis niloticus) during 18 days, in a recirculation system. The effects were measured by the proteic electrophoretic profile and the difference between the genders. One hundred twenty-six fish were used, 60 males and 66 females, both averaging 800g. The chronic hypoxia stress altered (P<0.05) the relative values of albumin, α+β-globulins, and γ-globulin; modified (P<0.05) the levels of total protein due to an increase in the male group; significantly decreased of the absolute mean values of albumin due to a decrease in the female group; and decreased the g-globulin values in males. The proteic profile, albumin, and γ-globulin were influenced by gender.

Kinetics of keratocyte proliferation in response to epithelial debridement.

Over the past 40 years, several groups have shown that epithelial debridement results in the death of keratocytes subjacent to the wound area. More recently this cell death has been shown to involve apoptosis. The purpose of this project was to examine the proliferative response of the normally quiescent keratocytes to repopulate the apoptotic area. Three mm wounds were made in the central cornea of adult rats and allowed to heal 4 hr to 14 days. Cryostat sections were stained with propidium iodide to mark the nuclei of all cells. Actively proliferating cells were identified with anti-Ki67, a marker of the late G1-M phase of the cell cycle. Anti-alpha-smooth muscle actin was used to determine if myofibroblasts were present. In unwounded corneas, keratocytes were uniformly spread throughout the stroma, and less than one proliferating cell per mm was observed. By 4 hr after wounding, the anterior one-half to three-fourths of the stroma subjacent to the wound was devoid of cells. No increase in Ki67-expressing cells was observed in the stroma until 24 hr after wounding (3.9 +/- 0.5 and 6. 3 +/- 0.5 mm(-1)in the wound center and edge, respectively). The number of Ki67-expressing cells steadily increased, peaking 44 hr after debridement (41.2 +/- 1.7 and 39.6 +/- 1.0). These cells were confined to a narrow zone adjacent to the area of cell death. No change in the number of cells expressing Ki67 was observed in the keratocytes distal to the original debridement. Ki67 levels did not return to control levels until 7 days after wounding. No alpha-smooth muscle actin was detected at any time point. This study indicates that epithelial debridement stimulates a synchronous increase in keratocyte proliferation. This stimulation is specific for cells immediately adjacent to the area of cell death. This activation does not involve the transformation of the stromal cells to a myofibroblast phenotype.