Dataset Information

Perinatal Exposure to Tartrazine Triggers Oxidative Stress and Neurobehavioral Alterations in Mice Offspring.

ABSTRACT: The use of synthetic azo dyes as coloring agents in food products has dramatically increased. This study evaluated the effect of perinatal exposure to tartrazine (TZ) on mice offspring, focusing on neurobehavioral alterations and oxidative stress. The female mice received TZ (2.5 and 5 mg/kg) via oral gavage during pregnancy and the first 15 days after birth. At days 21 and 35 after birth, male mice were sacrificed, and samples were collected for analyses. Perinatal exposure to TZ triggered tissue injury evidenced by the histological alterations and neuronal damage in the cerebrum, medulla oblongata, and cerebellum. TZ provoked lipid peroxidation and diminished cellular antioxidants in different brain regions of the newborns. In addition, TZ increased hemoglobin content, as well as erythrocytes, leukocytes, and platelets count at days 21 and 35 after birth. Both the locomotor behavior and anxiety reflex were significantly altered in mice exposed to TZ. In conclusion, perinatal exposure to TZ within an adequate daily intake range induced oxidative stress and neurobehavioral and hematological alterations in mice offspring. Therefore, consuming foods containing TZ during pregnancy and lactation warrants public awareness.

SUBMITTER: Albasher G

PROVIDER: S-EPMC7023231 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Perinatal Exposure to Tartrazine Triggers Oxidative Stress and Neurobehavioral Alterations in Mice Offspring.

Albasher Gadah G Maashi Najla N Alfarraj Saleh S Almeer Rafa R Albrahim Tarfa T Alotibi Fatimah F Bin-Jumah May M Mahmoud Ayman M AM

Antioxidants (Basel, Switzerland) 20200108 1

The use of synthetic azo dyes as coloring agents in food products has dramatically increased. This study evaluated the effect of perinatal exposure to tartrazine (TZ) on mice offspring, focusing on neurobehavioral alterations and oxidative stress. The female mice received TZ (2.5 and 5 mg/kg) via oral gavage during pregnancy and the first 15 days after birth. At days 21 and 35 after birth, male mice were sacrificed, and samples were collected for analyses. Perinatal exposure to TZ triggered tiss ...[more]

PMID: 31936188

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Project description:ObjectiveTo study the association between nicotine or cannabis metabolite presence in maternal urine and child neurodevelopmental outcomes.MethodsWe conducted a secondary analysis of two parallel multicenter randomized controlled trials of treatment for hypothyroxinemia or subclinical hypothyroidism among pregnant individuals enrolled at 8-20 weeks of gestation. All maternal-child dyads with a maternal urine sample at enrollment and child neurodevelopmental testing were included (N=1,197). Exposure was urine samples positive for nicotine (cotinine) or cannabis 11-nor-9-carboxy-delta-9-tetrahydrocannabinol [THC-COOH]) or both metabolites. Primary outcome was child IQ at 60 months. Secondary outcomes included cognitive, motor and language, attention, behavioral and social competency, and differential skills assessments at 12, 24, 36, and 48 months. Quantile regression analysis was performed with confounder adjustment.ResultsOf 1,197 pregnant individuals, 99 (8.3%) had positive cotinine samples and 47 (3.9%) had positive THC-COOH samples; 33 (2.8%) were positive for both. Groups differed in self-reported race and ethnicity, education, marital status, insurance, and thyroid status. Median IQ was similar between cotinine-exposed and -unexposed children (90 vs 95, adjusted difference in medians -2.47, 95% CI -6.22 to 1.29) and THC-COOH-exposed and -unexposed children (89 vs 95, adjusted difference in medians -1.35, 95% CI -7.76 to 5.05). In secondary outcome analysis, children with THC-COOH exposure compared with those unexposed had higher attention scores at 48 months of age (57 vs 49, adjusted difference in medians 6.0, 95% CI 1.11-10.89).ConclusionsNeither prenatal nicotine nor cannabis exposure was associated with a difference in IQ. Cannabis exposure was associated with worse attention scores in early childhood. Longitudinal studies assessing associations between child neurodevelopmental outcomes and prenatal nicotine and cannabis exposure with a focus on timing and quantity of exposure are needed.Clinical trial registrationClinicalTrials.gov, NCT00388297.

Project description:BackgroundBy altering specific developmental signaling pathways that are necessary for fetal lung development, perinatal nicotine exposure affects lung growth and differentiation, resulting in the offsprings' predisposition to childhood asthma; peroxisome proliferator-activated receptor gamma (PPAR?) agonists can inhibit this effect. However, whether the perinatal nicotine-induced asthma risk is restricted to nicotine-exposed offspring only; whether it can be transmitted to the next generation; and whether PPAR? agonists would have any effect on this process are not known.MethodsTime-mated Sprague Dawley rat dams received either placebo or nicotine (1 mg/kg, s.c.), once daily from day 6 of gestation to postnatal day (PND) 21. Following delivery, at PND21, generation 1 (F1) pups were either subjected to pulmonary function tests, or killed to obtain their lungs, tracheas, and gonads to determine the relevant protein markers (mesenchymal contractile proteins), global DNA methylation, histone 3 and 4 acetylation, and for tracheal tension studies. Some F1 animals were used as breeders to generate F2 pups, but without any exposure to nicotine in the F1 pregnancy. At PND21, F2 pups underwent studies similar to those performed on F1 pups.ResultsConsistent with the asthma phenotype, nicotine affected lung function in both male and female F1 and F2 offspring (maximal 250% increase in total respiratory system resistance, and 84% maximal decrease in dynamic compliance following methacholine challenge; P < 0.01, nicotine versus control; P < 0.05, males versus females; and P > 0.05, F1 versus F2), but only affected tracheal constriction in males (51% maximal increase in tracheal constriction following acetylcholine challenge, P < 0.01, nicotine versus control; P < 0.0001, males versus females; P > 0.05, F1 versus F2); nicotine also increased the contractile protein content of whole lung (180% increase in fibronectin protein levels, P < 0.01, nicotine versus control, and P < 0.05, males versus females) and isolated lung fibroblasts (for example, 45% increase in fibronectin protein levels, P < 0.05, nicotine versus control), along with decreased PPAR? expression (30% decrease, P < 0.05, nicotine versus control), but only affected contractile proteins in the male trachea (P < 0.05, nicotine versus control, and P < 0.0001, males versus females). All of the nicotine-induced changes in the lung and gonad DNA methylation and histone 3 and 4 acetylation were normalized by the PPAR? agonist rosiglitazone except for the histone 4 acetylation in the lung.ConclusionsGermline epigenetic marks imposed by exposure to nicotine during pregnancy can become permanently programmed and transferred through the germline to subsequent generations, a ground-breaking finding that shifts the current asthma paradigm, opening up many new avenues to explore.

Dataset Information

Perinatal Exposure to Tartrazine Triggers Oxidative Stress and Neurobehavioral Alterations in Mice Offspring.

Publications

Perinatal Exposure to Tartrazine Triggers Oxidative Stress and Neurobehavioral Alterations in Mice Offspring.

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