Acrolein (Ac) is the second most commonly inhaled toxin, produced in smoke of fires, tobacco smoke, overheated oils, and fried foods; and usually associated with lung toxicity. Crocin (Cr) is a natural carotenoid with a direct antioxidant capacity. Yet, oral administration of crocin as a natural rout is doubtful, because of poor absorbability. Therefore, the current study aimed to compare the potential protective effect of oral versus intraperitoneal (ip) crocin in mitigating Ac-induced lung toxicity. 50 Adult rats were randomly divided into 5 equal groups; Control (oral-saline and ip-saline) group, Cr (oral-Cr and ip-Cr) group, Ac group, oral-Cr/Ac group, and ip-Cr/Ac group; for biochemical, histopathological, and immunohistochemical investigations. Results indicated increased oxidative stress and inflammatory biomarkers in lungs of Ac-treated group. Histopathological and immunohistochemical examinations revealed lung edema, infiltration, fibrosis, and altered expression of apoptotic and anti-apoptotic markers. Compared to oral-Cr/Ac group, the ip-Cr/Ac group demonstrated remarkable improvement in the oxidative, inflammatory, and apoptotic biomarkers, as well as the histopathological alterations. In conclusion, intraperitoneal crocin exerts a more protective effect on acrolein-induced lung toxicity than the orally administered crocin.

Atrazine (ATR) is an extensively used herbicide that is often found in drinking water and waterways. After metabolization and excretion in the liver, ATR residues or its metabolites were found in tissues causing harmful effects mainly to the endocrine system and liver. This study aimed to elucidate the toxic impact of ATR on the liver and possible ameliorative effects of L-carnitine (LC). It utilized 30 adult male albino rats divided into three equal groups; the control group received 0.5 cc distilled water orally for 14 days, an ATR-treated group received ATR in a dose of 400 mg/kg BW dissolved in distilled water by oral gavage daily for 14 days, and a protected group (ATR + LC) received 400 mg/kg BW of ATR dissolved in distilled water, plus 100 mg/kg LC dissolved in distilled water by oral gavage daily for 14 days. At the end of the experiment, the liver tissue was prepared for histological and biochemical analyses and showed significant elevation of liver enzymes and oxidative parameters, altered expression of apoptotic and antiapoptotic genes, and hepatic degenerative changes in the ATR-treated group. In conclusion, atrazine induces oxidative stress, inflammation, and apoptosis in the liver of rats, and these toxic effects can be alleviated by L-carnitine.

Lambda-cyhalothrin (LCT) is one of the most frequently utilized pyrethroids. This study aimed to explore the toxic effects of subacute exposure to LCT on the pancreas and the hepatic glucose metabolism in adult male albino rats. 20 rats were equally grouped into; Control group and LCT group. The latter received LCT (61.2 mg/kg b.wt.), orally on a daily basis for 28 days. At the end of experiment, blood samples were collected for the determination of serum glucose and insulin levels. Pancreases were harvested and levels of malondialdehyde (MDA); catalase (CAT); superoxide dismutase (SOD); reduced glutathione (GSH); tumor necrosis factor-α (TNF-α); interleukin-6 (IL-6); nuclear factor erythroid 2–related factor 2 (Nrf2); heme oxygenase 1 (HO-1); and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were assessed. Also, liver samples were analyzed for the activity of glucose metabolism enzymes, glycogen content, and pyruvate and lactate concentrations. Histopathological and immunohistochemical examinations of pancreatic tissues were undertaken as well. Results revealed hyperglycemia, hypoinsulinemia, increased MDA, TNF-α, IL-6, and NF-κB levels, in association with reduced CAT, SOD, GSH, Nrf2, and HO-1 levels in LCT group. Liver analyses demonstrated a clear disturbance in the hepatic enzymes of glucose metabolism, diminished glycogen content, decreased pyruvate, and increased lactate concentrations. Besides, pancreatic islets displayed degenerative changes and β-cells loss. Immunohistochemistry revealed diminished area percentage (%) of insulin and Nrf2 and increased TNF-α immunoreaction. In conclusion, subacute exposure to LCT induces pancreatic toxicity, mostly via oxidative and inflammatory mechanisms, and dysregulates hepatic glucose metabolism in albino rats.

Tributyltin (TBT) is an organotin compound widely used as a biocide in antifouling paints. Moringa oleifera oil (MOO) has a promising antioxidant potential, which necessitates further exploration. This study was conducted to investigate the potential protective effect of MOO against TBT‐induced brain toxicity. The 30 rats were grouped into five groups (six each), Group I negative control, Group II positive control (vehicle), Group III MOO (5 ml/kg body weight [b.wt.]), Group IV TBT (10 mg/kg b.wt.), and Group V TBT & MOO. All treatments were given orally for 28 days. Thereafter, brains were exposed to oxidative stress and neurological parameters analyses. Histopathological and immunohistochemical (caspase‐3, Bax, Bcl‐2) examinations were also carried out. In rats administered TBT, increased malondialdehyde level, decreased reduced glutathione, and low total antioxidant capacity levels were in support of oxidative stress mechanism. Neurotoxicity was indicated by high nitric oxide level and increased acetylcholinestrase activity. Along with the histopathological alterations, the dysregulated expression of caspase‐3, Bax, and Bcl‐2 were indicative of the apoptotic mechanism mediated by TBT. Co‐administration of MOO with TBT ameliorated the aforementioned toxic effects. In conclusion, TBT causes brain toxicity via oxidative, nitrosative, and apoptotic mechanisms. MOO demonstrates protective effect against TBT‐induced brain toxicity mostly via potent antioxidant and antiapoptotic properties.

Little knowledge is available about the effects of fluoride exposure on the tongue. This study evaluated the effects of sodium fluoride (NaF) on the tongue ultrastructure and detected the ameliorative effects of resveratrol. Forty adult albino rats were separated into 4 groups: the control group was given a balanced diet and purified water. The NaF treated group: received 10 mg/kg/d dissolved in 2.5 ml distilled water once daily for 30 days orally. The NaF+resveratrol group: received NaF 10 mg/ kg/d orally together with resveratrol in a dose of 30 mg/kg daily for 30 days. The resveratrol group was subjected to resveratrol in a dose of 30 mg/kg/d by oral gavage for 30 days. Sections were stained with hematoxylin & eosin, and Masson's trichrome. Tumor necrosis factor α immunohistochemical study and electron microscopic examinations were done. The oxidative stress markers malondialdehyde, antioxidant reduced glutathione, and the total antioxidant capacity were measured. The NaF group revealed ulceration, necrotic muscle fibers, distorted papillae and a significant increase in malondialdehyde level, and a significant decrease in glutathione and the total antioxidant levels. In the NaF+resveratrol group, pathological changes were less, and the oxidant levels were decreased by the administration of resveratrol with NaF. In conclusion, NaF adversely affects the ultrastructure of the adult rat tongue and resveratrol can ameliorate this effect.

No abstract

Vigabatrin (VGB) is an effective antiepileptic drug used mainly to treat infantile spasms and refractory complex partial seizures. However, using VGB was restricted as it was known to cause retinal toxicity that appears as a severe peripheral visual field defect. Accordingly, this study was conducted to examine the histopathological and biochemical effects of VGB on the retina in adult male albino rats and assess the possible therapeutic role of mesenchymal stem cells (MSCs) against this potential toxicity. The rats were divided into three groups (control group, VGB group, and VGB/MSCs group), one week after 65 days of VGB treatment ±MSCs. The right eyeballs were prepared for histological and immunohistochemical examination, whereas the left eyeballs were prepared for real-time polymerase chain reaction analysis. Our results demonstrated that MSCs ameliorated retinal pathological changes and downregulated the expression of glial fibrillary acidic protein, vascular endothelial growth factor, and synaptophysin after VGB administration suggesting MSCs function and vascular modulating effect. Moreover, MSCs regulate retinal tissue gene expression of BAX, Bcl-2, BDNF, NGF, synapsin, interleukin (IL)-6, IL-1β, and occludin suggesting MSCs antiapoptotic and immunomodulating effect. In conclusion, MSCs administration could be a suitable therapeutic line to ameliorate VGB-induced retinopathy.