Time Course of Serum S100B Protein and Neuron‐Specific Enolase Levels of a Single Dose of Chlorpyrifos in Rats

Abstract

Organophosphate (OP) compounds are a large class of chemicals, many of which are used as pesticides. It is suggested that OPs specifically affect glia and neurons. Effects of acute exposure to chlorpyrifos (CPF), which is a common organophosphorus pesticide used worldwide, on neuron-specific enolase (NSE) and S100B levels in rat blood during 7 days were assessed. Rats were evaluated either before (0 hr) or 2, 12, 24, 48 and 168 hr (7 days) after injection of CPF (279 mg ⁄ kg, s.c.) or vehicle (peanut oil, 2 ml ⁄ kg, s.c.) for clinical signs of toxicity. Immediately after the evaluation of toxicity, blood samples were taken for biochemical assays. CPF administration produced decreases in body-weight and temperature, which were observed for first time at 12 hr after CPF administration and continued for 168 hr (p < 0.05-0.001). Serum S100B and NSE levels were acutely increased 2 hr after CPF administration and remained high at 12 hr (p < 0.01-0.001). NSE and S100B levels were not different in either CPF or vehicle groups at following time points. Serum butyrylcholinesterase (EC 3.1.1.8; BuChE) activity was dramatically reduced at 2 hr after CPF and remained low at each time points during 7 days (p < 0.01-0.001). Our results suggest that the usefulness of serum levels of these glia-and neuron-specific marker proteins in assessing OP toxicity, specifically CPF-induced toxicity.

Prediction of Acute Organophosphate Poisoning Using Glasgow Coma Sale, Serum Cholinesterase and S100B

“…As regard, serum S100B level at both admission and after 24hrs, this study revealed significant increase in its level in died patients than survived patients although, it cannot predict mortality. Bozkurt et al, (2010) reported that S100B level was elevated 2 h after exposure to chlorpyrifos in adult rats revealing usefulness of it in assessment of OP toxicity. Additionally, Yardan et al, (2013) detected that S100B level was significantly elevated in nonsurvivors.…”

“…Schwann cells), and S-100BB (astroglial cells) (Bottiger et al, 2001). S100B is expressed mainly in astrocytes of the central nervous system (CNS) (Yardan et al, 2009;Bozkurt et al, 2010). S100B is an established peripheral biomarker of blood-brain-barrier permeability associated with various CNS injuries or degeneration such as traumatic cortical injury and cerebrovascular insults as well as in some psychiatric disorders (Rothermundt et al, 2003), cardiac arrest or surgery (Qiao et al, 2001;Caughlan et al, 2004).…”

“…S100B is an established peripheral biomarker of blood-brain-barrier permeability associated with various CNS injuries or degeneration such as traumatic cortical injury and cerebrovascular insults as well as in some psychiatric disorders (Rothermundt et al, 2003), cardiac arrest or surgery (Qiao et al, 2001;Caughlan et al, 2004). Normal levels reliably exclude major CNS pathology (Guizzetti et al, 2005;Bozkurt et al, 2010). S100B may be a potential new marker in clinical toxicology; it was associated with level of consciousness in carbon monoxide poisoning, benzodiazepine, and aluminum phosphide toxicity (Ambrozic et al, 2008;Yardan et al, 2009;Cakir et al, 2010;Shahin et al, 2016).…”

Toxicity Assessment of Sub Lethal Doses of Chlorpyrifos on the Kidney and Liver Organs of Male Wistar Rats

“…Jaiswal and Verma [34][35][36] also reported that the most profound rat stress was the reduction of body weight after administration of chlorpyrifos. Studies conducted by [37][38][39] gave decreased body weights in rats treated with chlorpyrifos with no effects on physical or reflex development. This present study also revealed leucopenia in packed cell volume (PCV) which was apparently due to lymphopenia, neutropenia, and monocytopenia in the chlorpyrifos animal treated groups.…”

S100B is required for maintaining an intermediate state with double-positive Sca-1+ progenitor and vascular smooth muscle cells during neointimal formation

“…Stromal cell-derived factor-1 α (SDF-lα), one of the crucial signal molecules and landmarks of cell migration, was actually involved in triggering migration of Sca-1+ progenitor cells into the neointima by activating its receptor CXCR4 in the process of neointimal formation after vessel damage [20]. Considering the traits of common action of S100B and SDF-lα as inflammatory factors, S100B levels reached the peak at 2–6 h after tissue injury [21, 22], while SDF-lα expressions peaked 24 h after heart and vessel injury [23, 24], indicating that S100B could have a potential role in inducing SDF-lα expression in the injured vessels, and involving in the development of neointimal formation through SDF-lα signaling.…”