Investigation of inflamatory and oxidative parameters in female rats exposed to endotoxins during fetal and pubertal period

Investigation of Inflamatory and Oxidative Parameters in Female Rats Exposed to Endotoxins During Fetal and Pubertal Period Aim: Effects of fetal and pubertal edotoxin exposure (or lipopolysaccharide, LPS) on inflammatory and oxydative stress parameters are not known. Aim of the current thesis was to investigate the effects of fetal and pubertal endoxin exposure on hematological parameters, TNF-alpha, IL-1beta, corticosterone, LH and FSH levels and tissue oxydative stress parameters in female rat pups. Material and method: Rats were injected intraperitoneally sterile saline (n=5) or endotoxin (n=5) on days 17-18 of pregnancy. Following birth, female pups were subdivided into two groups and injected either strerile saline (SF, n=17) or endotoxin (LPS, n=17) on postnatal day 60 and four experimental groups were formed (SF+SF, SF+LPS, LPS+SF ve LPS+LPS). Blood and tissue samples were taken 4 hours postinjection at prepubertal period. Hematologic parameters, corticosterone, IL-1beta, TNF-alpha were determined in blood; and oxidative stress parameters were studied in kidney, heart and liver of tissues. Results: Neutrophil % ratio of SF+SF group was lower than SF+LPS, LPS+SF and LPS+LPS groups (p=0.001). Corticosterone, LH and FSH levels were not differentbetween the groups but TNF-alpha level of LPS+LPS groups was higher than SF+SF and LPS+SF groups (p=0.005). IL-1beta level of SF+LPS group was however higher than SF+SF and LPS+SF groups (p<0.05). Heart tissue SOD levels in the LPS+SF groups was lower than the others groups (p=0.000). Conclusion: This results obtained suggest that (1) prenatal and pubertal endotoxine exposure increases neutrophil count without affecting hypothalamo-pituitary-adrenal and –gonadal axes, that (2) TNF-alpha response against endotoxins was due to prenatal programming whereas there was no such a programming for IL-1beta, that (3) oxydative stress parameters, except SOD level, were not affected by prenatal or postnatal endoxin exposure. Key words: Maternal exposure, endotoxin, oxydative stress, inflammation, rat