Studies Of Neurotoxic Effects Research Articles

Neurobehavioral Effects of Low-Dose Chronic Exposure to Insecticides: A Review.

The modes of action of insecticides frequently involve a neurotoxic effect; therefore, the study of neurotoxic effects caused by long-term and low-dose insecticide exposure is of particular interest. This study looks at whether or not new studies conducted after 2009 and up to 2021 have provided new evidence for a better understanding of the actual neurobehavioral risk associated with long-term insecticide exposure. We selected and reviewed studies carried out on the neurobehavioral effects of neurotoxic insecticides (organophosphates and/or carbamates, pyrethroids, multiple or undefined insecticides, and organochlorines) considering occupational and non-occupational exposures. The articles were also scored and ranked based on seven parameters. Eighty-six studies were chosen for a final review process from among the 950 scientific papers identified. Twenty-six addressed occupational exposure and six environmental exposure. Among the latter group of studies, 17 focused on rural residents, to be assumed exposed because of living in rural areas, and 43 on the general population. Pending doubts have not been resolved in the last ten years due to the presence of contradictory and hardly comparable results and the fact that in most of the studies showing an evident neurobehavioral impairment the frequent presence of a previous episode of poisoning and hospitalization, with severe brain hypoxia, impaired the possibility of confirming the presence of a causal association with insecticide exposure. Interestingly, the most severely exposed groups, such as applicators who did not wear personal protective equipment, performed worse on neurobehavioral tests. As for residential exposure, there is sufficient evidence to suggest that prenatal OP exposure may increase the risk of ADHD in children.

Study of neurotoxic effects and underlying mechanisms of aconitine on cerebral cortex neuron cells

The study investigated the neurotoxiceffects and underlying mechanisms of aconitine on cerebral cortex neuron cells prepared from neonatal SD rats. The uniform design and MTT method were applied to study the effect of aconitine with different concentrations at scheduled time. The influence of aconitine at the maximal toxicity concentration was observed using optical microscope and electron microscope. The influences of aconitine on neuron cells membrane, neuron cells' inner balance, energy metabolism and neurotransmitters were observed to investigate the action mechanisms of aconitine. The results indicated that the maximal toxicity-concentration was 2% and the critical time were 30 s, 1 min and 20 min respectively. The effects of aconitine on neuron cells' morphology included cells synapse's fracture, cells membrane fragment, mitochondria's swell, cytoplasmic vacuoles, nuclear chromatin's condensation and accumulation. The stability of biomembrane, the internal milieu and the energy metabolism were also disturbed with the increase of activity of LDH and concentration of neurotransmitters (acetylcholine, opioid, catecholamine and SP) in culture medium, the increase of the activity of ACP and [Na+], [Ca2+] concentration, and the decrease of Na(+)-K(+)-ATP, [K+], [Mg2+] and glycogen concentration in the cells. Toxic mechanisms of aconitine damaging neuron cells may be because it inhibited the activity of Na(+)-K(+)-ATP, influenced the concentrations of [Na+], [K+], [Ca2+], [Mg2+] and neurotransmitters in the cells, which resulted in the injuries of cells' morphology and function.

Early Diagnosis of the Effects of Long-Term Neurotoxic Action of Lead, Based on the Analysis of Heart Rate

A method for subclinical diagnosis of the consequences of exposure to lead with an example of heart rate analysis is substantiated, and methods for the study of neurotoxic effects on the autonomic nervous system are critically evaluated.

Precision of Benchmark Dose Estimates for Continuous (Nonquantal) Measurements of Toxic Effects

The benchmark dose (BMD) corresponding to a low level of the risk of induced disease, e.g., 1 to 10%, has been proposed by various authors as a replacement for the no observed adverse effect level for noncancer endpoints in the regulation of the conditions of exposure to chemicals. This paper focuses on the variability of estimates of the BMD for nonquantal (continuous measurements) of biological endpoints such as are encountered for hematological data, clinical chemistry, and studies of neurotoxic effects. For biological endpoints that can be described by a normal distribution, estimates of the mean and standard deviation are required to calculate the BMD. Estimates of the standard deviation generally are quite variable, particularly for small sample sizes. The purpose of this paper is to examine the precision of the estimates of risk and of the BMD resulting from the inherent variability of the estimates of the standard deviations particularly for bioassays that employ a small number of animals. When the standard deviation is underestimated, the BMD and the regulatory “safe” dose are underestimated. Conversely, when the standard deviation is overestimated, the BMD and safe dose are overestimated. Overestimation of the BMD can be reduced or eliminated by using a lower confidence limit. The worst cases arise where only a few animals are used per dose and the dose response is supralinear (changes rapidly at low doses and levels off at higher doses). If the standard deviation is constant across doses (for lognormally distributed data if the coefficient of variation is constant), a pooled estimate across doses of the standard deviation can be used. In this case, for bioassays employing a total of 40 to 50 animals, the calculation of the BMD will generally be within a factor of 2 of the true value. When the standard deviation is not constant across dose groups, it is desirable to have more than 10 animals per dose group.