Oxidative Stress and Apoptosis Biomarkers in Neonate Rats’ Brain Exposed to Diquat during Lactation | ||||
| The Egyptian Journal of Hospital Medicine | ||||
| Article 30, Volume 77, Issue 6, October 2019, Page 5989-5994 PDF (587.87 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/ejhm.2019.67316 | ||||
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| Abstract | ||||
| Background: Toxic chemicals compete with biological macromocules and other small molecules that construct brain structure in their natural function. Interruptions in development of the brain caused by toxic compounds, both before and after birth, can lead to defects that occur quickly after exposure, or much later in life. Objectives: This study aimed to throw light on the effect of diquat (DIQ) on the development of neonates, brain by determination of oxidative stress and apoptosis markers during lactation period. Materials and methods: Twenty pregnant female rats from the breeding facility of the Mammalian Toxicology Department, the Central Agricultural Pesticides Laboratory, Agriculture Research Center were included in this study. The lactating dams and their pups were constructed into two experimental groups (10 dams each). The first saved as a control group and received distilled water daily during the breast-feeding period. The second group was intubated with 5.12 mg/kg DIQ as 1/80 of LD50 (according to preliminary trails) from the 1st postnatal day (PND1) to the 10th postnatal day (PND10) and served as treated (study) group. Brain samples of neonates were collected after treated period and the 21th postnatal day (PND 21). The oxidative stress biomarkers (SOD, GPx, GST, GSH and Protein carbonyl) and gene expression of BAX and BCL2 as apoptosis markers were estimated. Results: The results indicated disruption in both oxidative stress and apoptosis biomarkers as evidenced by increased in GST, GPx activities, gene expression of BAX and protein carbonyl level. Also, results showed a decline in SOD activity, BCL-2 gene expression and GSH content declined. Conclusion: The results of this study showed that exposure to DIQ increases the generation of free radicals and can cause oxidative stress and induce neuronal programed cell death | ||||
| Keywords | ||||
| Diquat; Oxidative Stress; apoptosis; Gene expression; lactation; Neonates | ||||
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