Neurotoxicity of acrylamide in adult zebrafish following short-term and long-term exposure: evaluation of behavior alterations, oxidative stress markers, expression of antioxidant genes, and histological examination of the brain and eyes.

In the present work, 224 adult female zebrafish (56 fish in each group) were randomly divided into four groups (two control groups and two toxicity groups) as per duration of exposure (7 and 21 days). All fish of the two toxicity groups were exposed to 0.610 mM acrylamide (ACR) concentration for 7 and 21 days. The effects of ACR exposure on behavior, oxidative stress biomarkers, molecular expression of antioxidant genes (sod, cat, and nrf2), and histopathological examination of the brain and eye were examined. Our result shows that ACR exposure for 7 days produced an anxiety-like behavior in zebrafish. Short-term exposure of ACR resulted in alterations of oxidative stress markers (SOD and CAT activity, and the level of GSH and MDA) in the brain and eye of zebrafish. However, the antioxidant defense system of adult female zebrafish could be able to counteract the free radicals generated in long-term ACR exposure as indicated by non-significant difference in oxidative insult following short-term and long-term exposure. ACR exposure downregulated the mRNA expression of the sod, cat, and nrf2 (nuclear factor erythroid 2-related factor 2) genes in the brain and eye without significant difference between the two toxicity groups. Mild histological changes in the dorsal telencephalic area, tectum opticum, medulla, and hypothalamus area of the brain of zebrafish have been observed following short-term and long-term ACR exposure. In the eye, marked histological changes in the retinal pigmented epithelium layer (RPE), structural changes of the photoreceptor layer (PRL) with disorganized layer of rods and cones, and reduction of the relative thickness of the RPE, PRL, outer nuclear layer (ONL), and inner nuclear layer (INL) have been noted following ACR exposure for 21 days as compared to 7 days. ACR produced neurobehavioral aberrations and oxidative stress within 7 days of exposure, while various histological changes in the brain and eyes have been observed following long-term exposure (21 days) to ACR.

Toxicopathological evaluation in Wistar rats (Rattus norvegicus) following repeated oral exposure to acephate.

The present study was carried out to evaluate the effects of exposure at different doses of acephate on hematology, blood biochemistry, oxidative stress and immune system of Wistar rats. The experiment was carried out on 40 Wistar rats, which were divided in four groups. Animals of the three treatment groups were given with different sublethal doses (1/40th, 1/20th, 1/10th of lethal dose 50 value) of acephate by oral gavage. The hematology, blood biochemistry, oxidative stress marker, humoral immune response and cell-mediated immunity were evaluated following acephate exposure. Significant alteration in hematological parameters was not observed following different doses of acephate; however, significant alteration in alkaline phosphatase, gamma glutamyl transferase, acetyl cholinesterase, lipid peroxidase and superoxide dismutase was observed in medium- and high-dose group animals. Nonsignificant decrease in antibody titer in animals exposed to high dose has been observed compared with animals of control group. However, significant alteration in cell-mediated immunity was not observed in animals treated with acephate at different doses.