Prenatal Exposure to Nicotine in Pregnant Rat Increased Inflammatory Marker in Newborn Rat

Abstract

This study aimed to investigate any inflammatory effect of nicotine on rat embryo by exposing their mothers to different dosages of nicotine during pregnancy. During this experimental study, 32 pregnant healthy Wistar rats were divided into 4 equal groups, including a control and 3 nicotine exposure groups. Injections were performed subcutaneously starting at the first day of pregnancy until parturition. As the dosages of nicotine were increased, the weight gain by pregnant rats and the mean weight of their newborns were significantly reduced. Mean ± SD of hs-CRP was significantly higher among groups exposed to various dosages of nicotine (2, 4, and 6 mg/kg) compared to the control group (P < 0.0001) and its increasing rate was also dose dependent. Mean ± SD serum level of IL-6 and TNF-α among all groups exposed to nicotine, except for 2 mg/kg nicotine injected group, was increased significantly (P < 0.0001). Mean ± SD of serum level of TGF-β and nitrite oxide among exposure groups showed significant differences compared to the control group only at the dosage of 6 mg/kg (P < 0.0001). The current study showed that exposing pregnant rats to nicotine causes a dose dependent increase in the rate of all the studied inflammatory serum markers among their newborns.

α7 nAChR mediated Fas demethylation contributes to prenatal nicotine exposure-induced programmed thymocyte apoptosis in mice

“…Prenatal cigarette smoke exposure could induce thymus atrophy in the fetus and result in allergy-prone deviation in the T-cell response, which manifests as increased IL-4 production during allergic disease development, in postnatal life [ 28 , 41 , 42 ]. Evidence also showed that PNE is related to increased production of inflammatory cytokines after birth [ 43 ]. Additionally, Abbas and Vadesilho reported that the increased IL-4 production could cause an abnormal increase of the ratio of IgG1/IgG2, which in turn polarized the offspring immune system toward immune diseases [ 44 , 45 ].…”

Prenatal and lactation nicotine exposure affects Sertoli cell and gonadotropin levels in rats

“…In contrast to necrosis, which has been described to be a consequence of extreme physicochemical stress that leads to an accidental and uncontrolled phenomenon (Vanden Berghe et al 2013), necroptosis is a programmed necrosis that promotes inflammation through leakage of cellular content from damaged plasma membranes . Interestingly, the exposure of pregnant rats to nicotine causes a dose dependent increase in the rate of inflammatory serum markers in the progeny (Mohsenzadeh et al 2014). Thus, it is possible that some cells observed in the current study, which presented suggestive morphological characteristics of death, could be cells in necroptosis.…”

Alteration of fibronectine expression in the kidney extracellular matrix following nicotine administration in gestation and lactation period

“…Presumably the cooperation of Connective-Tissue Growth Factor with TGFβ-1 induces the expression of extracellular matrix components (Mendes et al, 2015). So kidney fibroblasts that synthesis high levels of fibronectine mRNA activate with TGFβ (Mohsenzadeh et al, 2014). Also maternal nicotine administration during prenatal and postnatal induces epithelium to mesenchym transformation and cause fibrosis in offspring organs (Chen et al, 2015).…”