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Sharma et al. Zinc supplementation prevents against LPS induced neurotoxicity in rats

levels in prenatally IL-1β exposed female pups were 8. Romero R, Roslansky P, Oyarzun E, Wan M, Emamian M, Novitsky
observed due to decrease in progesterone turnover TJ, Gould MJ, Hobbins JC. Labor and infection. II. Bacterial
to its metabolites in hippocampus which was not the endotoxin in amniotic fluid and its relationship to the onset of preterm
labor. Am J Obstet Gynecol 1988;158:1044-9.
same in case of male pups. However, this could also 9. Gendron RL, Nestel FP, Lapp WS, Baines MG. Lipopolysaccharide-
be related to differential increase of NE levels in case induced fetal resorption in mice is associated with the intrauterine
of pups of both sexes as observed in the present study. production of tumour necrosis factor-alpha. J Reprod Fertil
Results from histopathological studies were also in line 1990;90:395-402.
with the above discussed results. Therefore, it can be 10. Ogando DG, Paz D, Cella M, Franchi AM. The functional role of
suggested that LPS exposure prenatally effects pups increased production of nitric oxide in lipopolysaccharide-induced
embryonic resorption in mice. Reproduction 2003;125:95-110.
and is gender specific and the same is the case with 11. Leazer TM, Barbee B, Ebron-McCoy M, Henry-Sam GA, Rogers JM.
Zinc supplementation. Role of the maternal acute phase response and tumor necrosis factor
alpha in the developmental toxicity of lipopolysaccharide in the CD-1
Authors’ contributions mouse. Reprod Toxicol 2002;16:173-9.
Study planning and experimental design: B. Nehru, N. 12. Zhao L, Chen YH, Wang H, Ji YL, Ning H, Wang SF, Zhang C,
Sharma Lu JW, Duan ZH, Xu DX. Reactive oxygen species contribute
Experimental work and preparation of Tables and to lipopolysaccharide-induced teratogenesis in mice. Toxicol Sci
Figures: P. Arora, N. Sharma 2008;103:149-57.
Evaluation of the results: B. Nehru 13. Rivera DL, Olister SM, Liu X, Thompson JH, Zhang XJ, Pennline K,
Azuero R, Clark DA, Miller MJ. Interleukin-10 attenuates experimental
Manuscript writing and communication: N. Sharma fetal growth restriction and demise. FASEB J 1998;12:189-97.
14. Buhimschi IA, Buhimschi CS, Weiner CP. Protective effect of
Financial support and sponsorship Nacetylcysteine against fetal death and preterm labor induced by
None. maternal inflammation. Am J Obstet Gynecol 2003;188:203-8.
15. Xu DX, Chen YH, Zhao L, Wang H, Wei W. Reactive oxygen species
Conflicts of interest are involved in lipopolysaccharide-induced intra-uterine growth
There are no conflicts of interest. restriction and skeletal development retardation in mice. Am J Obstet
Gynecol 2006;195:1707-14.
Patient consent 16. Xu DX, Wang H, Ning H, Zhao L, Chen YH. Maternally administered
lipopolysaccharide-induced
regulates
melatonin
differentially
There is no patient involved. proinflammatory and anti-inflammatory cytokines in maternal serum,
amniotic fluid, fetal liver, and fetal brain. J Pineal Res 2007;43:74-9.
Ethics approval 17. Xu DX, Wang H, Zhao L, Ning H, Chen YH, Zhang C. Effects of low-
Ethical approval was obtained prior to the dose lipopolysaccharide (LPS) pretreatment on LPS-induced intra-
commencement of the study. uterine fetal death and preterm labor. Toxicology 2007;234:167-75.
18. Xu DX, Chen YH, Wang H, Zhao L, Wang JP, Wei W. Tumor necrosis
factor alpha partially contributes to lipopolysaccharide-induced intra-
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