Erythropoiesis in the Rps19 disrupted mouse: Analysis of erythropoietin response and biochemical markers for Diamond-Blackfan anemia

The human ribosomal protein S19 gene (RPS19) is mutated in approximately 20% of patients with Diamond-Black fan anemia (DBA), a congenital disease with a specific defect in erythropoiesis. The clinical expression of DBA is highly variable, and subclinical phenotypes may be revealed by elevated erythrocyte deaminase (eADA) activity only. In mice, complete loss of Rps19 results in early embryonic lethality whereas Rps19(+/-) mice are viable and without major abnormalities including the hematopoietic system. We have performed a detailed analysis of the Rps19(+/-) mice. We estimated the Rps19 levels in hematopoictic tissues and we analyzed erythrocyte deaminase activity and globin isoforms which are used as markers for DBA. The effect of a disrupted Rps19 allele on a different genetic background was investigated as well as the response to erythropoietin (EPO). From our results, we argue that the loss of one Rps19 allele in mice is fully compensated for at the transcriptional level with preservation of erythropoiesis. (c) 2005 Elsevier Inc. All rights reserved

<em>Adenium obesum</em> flowers extract mitigates testicular injury and oxidative stress in streptozotocin-induced diabetic rats.

Background and Objective: Diabetes Mellitus (DM) is a major healthcare problem worldwide and considerable evidence proved its negative impact on the male reproductive system. Adenium obesum is an interesting medicinal plant with a wide range of bioactivities. The current study examined the protective effects of A. obesum flower extract (AOE) on testicular injury in streptozotocin (STZ)-induced type I diabetic rats. Materials and Methods: Diabetes was induced by a single injection of 50 mg kg(-1) STZ. Diabetic rats received 250 and 500 mg kg(-1) AOE for 21 days and samples were collected for analysis. Results: As compared to the diabetic control rats, treatment with AOE increased serum testosterone, Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH) levels, decreased testicular thiobarbituric acid reactive substances (TBARS) content, effectively enhanced reduced glutathione (GSH) content and superoxide dismutase (SOD) activity. Additionally, AGE effectively inhibited diabetes-induced testicular tissue injuryand prevented inflammatoryand apoptotic responses manifested by decreased TNF-alpha, IL-6 and Bax and increased Bcl-2. Conclusion: These results demonstrated that AGE mitigates testicular injury, oxidative stress, inflammatory response and apoptotic cell death in STZ-induced diabetic rats