Caspase 1, Caspase 3, TNF-alpha, p53, and Hif1-alpha gene expression status of the brain tissues and hippocampal neuron loss in short-term dichlorvos exposed rats

Abstract

Dichlorvos (DDVP) is an organophosphate compound that causes neurotoxicity. Apoptosis plays an important role in neurotoxic cell death in the brain. The aim of this study was to examine caspase 1, caspase-3 and also cell apoptosis related genes as p53, Tumor Necrosis Factor-alpha, Hypoxia Inducible Factor 1-alpha expressions in hippocampus, cerebellum, cortex, and to estimate total hippocampal neuron number in DDVP treated rats. Ten female albino rats were divided into control (n:5) and dose (n:5) groups. In dose group, single dose of DDVP (25 mg/kg) was administered to the animals via oral gavage. A week later, brains were removed and total neuron number was estimated in the left hippocampus using by optical fractionator method. The right part of the brain was used for gene expression analysis. In dose group, total hippocampal neuron number was significantly decreased compared to control group (p = 0.008). Caspase 1 and TNF-alpha gene expression were increased in all brain tissues and p53 gene expression was decreased in only hippocampus tissue in dose group. Short-term exposure to dichlorvos leads to neuronal loss in hippocampus and TNF-alpha rapidly and potently induces apoptosis and also several caspases as possible participants in the apoptotic cascade.

TNF-α increases the intrinsic excitability of cerebellar Purkinje cells through elevating glutamate release in Bergmann Glia

“…What is the functional consequence of TNF-α-induced intrinsic plasticity of PCs in the cerebellar cortex? Elevation of TNF-α concentration in the cerebellum has been implicated in cerebellar pathophysiological dysfunction 51 , 52 . The data presented here shows electrophysiological outcomes of TNF-α elevation in cerebellar circuits.…”

Role of p53, Mitochondrial DNA Deletions, and Paternal Age in Autism: A Case-Control Study

“…[9][10][11][12] Studies have linked p53 to developmental abnormalities 13 (see also Supplemental Table 5), and regions adjacent to 17p13.1 encoding for proteins with important roles in brain function and neurodevelopment (eg, axonal dynein heavy chain 2 and Na + /K + ATPase subunit β-2) and others have been found to be associated with autism (AU) (eg, ephrin-B3 14 ). Increased p53/Bcl2 protein ratios had been found in brain regions of a small set of autistic subjects [15][16][17] ; however, no characterization of posttranslational modifications or functional status of p53 was undertaken.…”

Carvacrol protects against λ‐Cyhalothrin‐induced hepatotoxicity and nephrotoxicity by modulating oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress, and autophagy

“…Numerous studies have shown that pyrethroid compounds, such as λ‐Cyhalothrin, induce inflammation by elevating the expression of pro‐inflammatory cytokines in various tissues. For example, Nilufer Yonguc et al 75 and Mostafalou et al 25 both reported that dichlorvos and malathion increased the levels of TNF‐α expression in rat brain and liver, respectively. In addition, Aouey et al 33 reported that λ‐Cyhalothrin up‐regulates the expressions of LPO, IL‐1β, IL‐6, and IFN‐γ in the liver.…”