CPF (chlorpyrifos) is an organophosphate pesticide used in agricultural and veterinary applications. Our experiment aimed to explore the effects of thymoquinone (TQ) and/or lycopene (LP) against CPF-induced neurotoxicity. Wistar rats were categorized into seven groups: first group served as a control (corn oil only); second group, TQ (10 mg/kg); third group, LP (10 mg/kg); fourth group, CPF (10 mg/kg) and deemed as CPF toxic control; fifth group, TQ + CPF; sixth group, (LP + CPF); and seventh group, (TQ + LP + CPF). CPF intoxication inhibited acetylcholinesterase (AchE), decreased glutathione (GSH) content, and increased levels of malondialdehyde (MDA), an oxidative stress biomarker. Furthermore, CPF impaired the activity of antioxidant enzymes including superoxide dismutase (SOD) and catalase (CAT) along with enhancement of the level of inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β. CPF evoked apoptosis in brain tissue. TQ or LP treatment of CPF-intoxicated rats greatly improved AchE activity, oxidative state, inflammatory responses, and cell death. Co-administration of TQ and LP showed better restoration than their sole treatment. In conclusion, TQ or LP supplementation may alleviate CPF-induced neuronal injury, most likely due to TQ or LPs’ antioxidant, anti-inflammatory, and anti-apoptotic effects.

Carbon tetrachloride (CCl₄) is a strong hepatotoxic agent. The ability of the anti-inflammatory agent, lactoferrin (LF), to alleviate hepatic inflammation in a Wistar rat model administered with carbon tetrachloride (CCl₄) was examined. Thirty male Wistar rats were segregated into 5 groups (6 rats per group): Control group, LF group (300 mg LF/kg b. wt daily for three weeks), CCl₄ group (1 ml CCl₄/kg b. wt once orally), LF-protected group (300 mg LF/kg b. wt daily for 3 weeks followed by 1 mL CCl₄/kg b. wt once orally), and LF-treated group (1 mL CCl₄/kg b.wt once orally followed by 300 mg LF/kg b. wt orally every day for three weeks). Erythrogram, leukogram, activity of oxidative stress markers (Superoxide dismutase [SOD], Glutathione peroxidase [GPx], and Malondialdehyde [MDA]), and expression of hepatic paraoxonase-1 (PON1), interleukin (IL)-1β, and IL-10 mRNA were determined. Histopathological examination of the hepatic tissue was carried out. CCl₄ caused liver injury, loss of liver antioxidant activity of SOD and GPx, and a significant increase in the level of malondialdehyde in the serum. Moreover, CCl₄ induced up-regulation of hepatic pro-inflammatory (IL-1β) factors, and down-regulation of anti-inflammatory (IL-10 and PON1) factors. Based on histopathological examination, the hepatic tissues had severe inflammation and were damaged. However, LF mitigated the liver damage, oxidative stress, and hepatotoxicity caused by CCl₄. Overall, these results suggest that LF-mediated immunological mechanisms alleviate CCl4-induced hepatic toxicity and provide a novel perspective on the potential use of LF for prophylactic and therapeutic applications in treating liver diseases.

Malathion is considered one of the vastest pesticides use all over the world. Malathion-inhalation toxicity commonly occurred in many occupational farmers. Therefore, this study aimed to ameliorate the possible malathion-induced pulmonary toxicity through thymoquinone administration. Forty animals were used to conduct our study, divided into five groups; G1 control group, G2 thymoquinone (50 mg/kg) group, G3 malathion group (animals inhaled 100 mg/ml/m³ for 15 min for 5 days/week for three weeks), G4 and G5 were subjected to the same malathion inhalation protocol beside oral thymoquinone administration at doses of 25 and 50 (mg/kg), respectively. Malathion-inhalation induced marked systemic toxicity as hepatotoxicity and nephrotoxicity associated with increased serum hepatic and renal enzymes, and hypersensitivity accompanied with increased total IgE serum level. The lung showed severe interstitial pneumonia associated with severe vascular damage and marked eosinophil infiltration. Moreover, the lung showed a marked decrease in the pulmonary surfactant protein, especially SP-D gene expression. While, thymoquinone treatment to malathion-inhaled animals decremented the following; hepatic enzymes and renal function tests, total IgE as well as pneumonia and hypersensitivity pathological features, and augmented the expression of SP-D. In conclusion, thymoquinone could be potentially used in pest control workers to ameliorate the systemic and pulmonary intoxication caused by one of the most field-used pesticides.

The ameliorative effects of Spirulina and Saccharomyces cerevisiae (S. cerevisiae) against fipronil toxicity in Nile tilapia fish were investigated. Fipronil is a kind of pesticide that is widely used in agriculture, thus this trial was conducted to evaluate the effect of fipronil on growth related parameters (final body weight, feed intake, weight gain, feed conversion ratio, specific growth rate, and protein efficiency ratio), hematology related parameters (RBCs, WBCs, hemoglobin, packed cell volume, and deferential leukocytic count), biochemistry related parameters (alanine aminotransferase, aspartate aminotransferase, total protein, albumin, urea, and creatinine), histopathology of liver, intestine, gills, and spleen, and gene expression of antioxidants, stress, inflammatory, apoptotic, and related to junction proteins genes as SOD and GPx, COX II, TNF-α, Casp-3, and Claudin-3, respectively, in Nile tilapia (Oreochromis niloticus). Four hundred and five Nile tilapia fish were distributed in a glass aquarium into nine groups according to the Spirulina and S. cerevisiae supplemented diets, with or without fipronil contaminated water. The classified groups are control, Sc: S. cerevisiae (4 g/Kg diet), Sp: Spirulina (1 g/100 g diet), Fb1: 0.0021 mg fipronil/L, ScFb1: S. cerevisiae (4 g/Kg diet) with 0.0021 mg fipronil/L, SpFb1: Spirulina (1 g/100 g diet) with 0.0021 mg fipronil/L, Fb2: 0.0042 mg fipronil/L, ScFb2: S. cerevisiae (4 g/Kg diet) with 0.0042 mg fipronil/L, and SpFb2: Spirulina (1 g/100 g diet) with 0.0042 mg fipronil/L. The results of the present investigation indicated the negative effect of fipronil on the growth performance parameters of Nile tilapia, which was confirmed by the results of hematology, biochemistry, and histopathology. In addition, the results of gene expression of antioxidants, stress, inflammatory, and apoptotic genes indicate the genotoxicity of fipronil. However, these negative effects were ameliorated by Spirulina and Saccharomyces dietary supplementation.

The objectives of our study were to determine the presence of Aflatoxin M1 (AFM1) in market milk in Aswan province, Egypt and studying the effect of addition of some strains of probiotics microorganisms on AFM1 level in milk. Between July and October 2018, 90 market milk samples (15 Ultra Heat Treated (UHT), 75 raw) were collected from different dairy shops in Aswan City, Egypt to be examined for AFM1 presence by rapid strip test and the results were confirmed by high-performance liquid chromatography (HPLC). The results revealed that all UHT milk samples were negative, while 37 (49%) raw milk samples were positive for AFM1 residues. All 37 positive milk samples were examined by HPLC to determine the level of AFM1. The results showed that the level of AFM1 ranged between 0.053 and 0.207 with mean ± SE of 0.1003 ± 0.008 ppb. Some probiotics strains were used to determine their effect on AFM1 by milk fermentation; the result showed that the probiotics have significant effect on the reduction of AFM1 level in milk (p < 0.05). Also, Public health importance of AFM1 was discussed. Presence of AFM1 in 49% of examined raw milk samples indicate widespread occurrence of AFM1 in market milk in Aswan province, Egypt which considered possible hazards for consumers, while the absence of AFM1 from UHT milk indicates that type of milk is safer. So, regular monitoring of AFM1 in market milk is necessary for evaluating their contamination status. Mixed starter culture of Lactobacillus bulgaricus and Streptococcus thermophilus could be used as a biological agent for the reduction of AFM1 in milk.