title: Glomerular response to adrenocortical hormone alone or in combination with selenomethionine.
abstract: Increased levels of glucocorticoids (GC) can result in major complications such hypertension and vascular injury. Chronically, this condition may lead to impairment of renal function. Glucocorticoid excess was considered the etiologic agent that triggers over production of reactive oxygen species (ROS). The mode of action of ROS was implicated to disrupt nitric oxide availability in the vascular endothelium, leading to vascular complications. To circumvent this damage attempts were made to use antioxidants in order to counter-balance the oxidative process. The objectives of this study were: (1) to establish an animal model of increased glucocorticoid levels by sustained delivery and (2) to determine if sustained delivery of selenomethionine in combination with glucocorticoids could protect kidney tubular structures using adult rats. Sixteen female rats were divided into four equal groups (control and 3 experimental groups implanted with tricalcium phosphate lysine drug delivery systems (TCPL) charged with either 50mg selenomethionine (Se), 50 mg corticosterone (C), or 50 mg of both C and Se). At the end of 24 days, the rats were sacrificed and both kidneys were removed for histopathological analysis. Quantitative analysis was performed on serum calcium levels, body weights and kidney weights in animals from all groups. Kidney slides were screened for possible structural damage. Sustained release of Se and Se+C resulted in a significant reduction of glomerular area (p < 0.05). Data obtained indicated that C, Se and Se+C administration caused a reduction in serum calcium levels compared to control animals. The reduction may be in part to changes in calcium-filtered load, changes in glomerular filtration rates or interference of calcium absorption from the gut. In conclusion, data obtained from this investigation provided the literature with significant information regarding the role of sustained delivery of supraphysiological levels of corticosterone in modifying kidney structure and function (possibly alter blood pressure).
authors.affiliation: University of Mississippi Medical Center Jackson, MS 39216, USA.
authors.forename: Ham
authors.initials: H
authors.lastname: Benghuzzi
authors.forename: Michelle
authors.initials: M
authors.lastname: Tucci
authors.forename: James
authors.initials: J
authors.lastname: Hughes
authors.forename: Russell
authors.initials: R
authors.lastname: Lyon
authors.forename: Stevie
authors.initials: S
authors.lastname: Adams
mesh_terms: D000305:Adrenal Cortex Hormones / Q000008:administration & dosage; D000818:Animals; D001835:Body Weight / Q000187:drug effects*; D002118:Calcium / Q000097:blood*; D003345:Corticosterone / Q000008:administration & dosage*; D004338:Drug Combinations; D004343:Drug Implants / Q000008:administration & dosage*; D005260:Female; D007668:Kidney / Q000187:drug effects* / Q000473:pathology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012645:Selenomethionine / Q000008:administration & dosage*
chemical_list: D000305:Adrenal Cortex Hormones; D004338:Drug Combinations; D004343:Drug Implants; D012645:Selenomethionine; D002118:Calcium; D003345:Corticosterone