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Background: In third-world countries, poisoning due to dichlorvos (DDVP), an organophosphate insecticide, is prevalent due to its widespread usage in household and agriculture, with the brain bearing the brunt of the consequences. Hence, this study assessed the likely beneficial impact of hesperidoside (HESP) on the DDVP-mediated cerebral dysfunction in rat model. Method: Randomization was employed to earmark forty-two rats into seven groups: control, DDVP alone (8 mg.kg⁻¹day⁻¹), DDVP plus HESP (50 and 100 mg.kg⁻¹day⁻¹) and reference drug atropine (0.2 mg.kg⁻¹day⁻¹), and HESP alone (50 and 100 mg.kg⁻¹day⁻¹). Results: HESP intervention remarkably (p < 0.05) mitigated DDVP-potentiated augmentations in cerebral concentrations of H₂O₂, NO, and malondialdehyde; impaired DDVP-induced decrease in cerebral GSH, GST, SOD, catalase, glutathione peroxidase, and acetylcholinesterase; significantly (p < 0.05) suppressed DDVP-invoked upregulation of mRNA expression of NF-κB-p65, p53, BAX, caspase-3, and TNF-α; and significantly (p < 0.05) revoked DDVP-incited downregulation of interleukin-10. Conclusion: HESP chemotherapeutic interventions enhanced cerebral functions in DDVP-treated rats by abrogating oxidative stress, acetylcholinesterase inhibition, and NF-κB-p65/p53/caspases-3 signaling.

The contamination of edible agricultural goods with pesticides, including dichlorvos (DVDP), poses a substantial public health risk, promoting severe morbidity and mortality, especially in developing countries. It has been shown that hesperidin (hesperetin-7-O-rhamnoglucoside or Hes-7-RGlc) preserves cytomembrane, redox, and lipid homeostasis; unfortunately, its function on dichlorvos-incited heart damage has not been investigated. This work explored the ameliorative influence of Hes-7-RGlc on DVDP-activated cardiotoxicity. For this end, forty-two rats were randomly appropriated into seven groups (6 rats/group): Control, DVDP alone (8 mg.kg⁻¹day⁻¹), DVDP supplied with either Hes-7-RGlc (50 and 100 mg.kg⁻¹day⁻¹) or the reference medication atropine (0.2 mg.kg⁻¹day⁻¹), and Hes-7-RGlc alone (50 and 10 mg.kg⁻¹day⁻¹) were the seven groups investigated. DVDP was administered orally for seven days, followed by fourteen days of Hes-7-RGlc therapy. Then the rats were euthanized, and their blood and hearts were removed. Hes-7-RGlc chemotherapy substantially (p

Hepatocellular carcinoma is a prevalent form of liver cancer that is life threatening. Many chemically synthesized anti-cancer drugs have various degrees of side effects. Hence, this study investigated the effect of FEAC interventions on NDEA-CCl4-induced HCAR in male Wistar rats. HCAR was induced by intraperitoneal administration of 200 mg/kg of NDEA and 0.5 mL/kg CCl4 (as a promoter of HCAR). Following the induction of HCAR, rats were treated differently with two different doses (25 and 50 mg/kg) of FEAC. HCAR induction was confirmed by the significant elevation of serum levels of ALT, AST, and α-FP. Also elevated significantly were liver levels of Akt/PKB, NF-κB, TNF-α, MDA, GSH, and activities of GST, SOD, and CAT, while levels of liver p53 and Nrf2 were significantly lowered compared with normal rats. Treatment interventions with both 25 and 50 mg/kg of FEAC against the DEN-CCl4-induced HCAR gave comparable effects, marked by a significant reduction in the levels of serum ALT, AST and α-FP, as well as liver levels of MDA, GSH, Akt/PKB, NF-κB, TNF-α, GST, SOD, and CAT, while levels of liver p53 and Nrf2 were significantly elevated compared with normal rats. Put together and judging by the outcomes of this study, FEAC being a potent antioxidant may also be potent against chemical-induced HCAR via upregulation of p53 and Nrf2, as well as downregulation of the Akt/PKB-NF-κB pathway in rats.

Palm oil (PO), the most consumed edible oil, is persistently adulterated with Sudan IV dye (S4D). We investigated the potential hematological derangements occasioned by ingesting S4D-adulterated PO. Thirty male albino rats were grouped into five (n = 6); Control, PO (10%), PO + S4D (100 mg), PO + S4D (250 mg), and S4D (250 mg). Rats received unadulterated or S4D-adulterated PO through diet for 21 days. Exposure to S4D (alone and via adulterated PO) provoked significant (p 0.05) in the unadulterated PO-exposed rats compared to the control. These results reveal the potential hematotoxic and immunotoxic effects of adulterating PO with S4D.

Earlier reports have shown that Cyclophosphamide (CYCP), an anti-malignant drug, elicited cytotoxicity; and that naringin has several beneficial potentials against oxidative stress and dyslipidaemias. We investigated the influence of naringin on free radical scavenging, cellular integrity, cellular ATP, antioxidants, oxidative stress, and lipid profiles in the CYCP-induced erythrocytotoxicity rat model. Rats were pretreated orally by gavage for fourteen consecutive days with three doses (50, 100, and 200 mg/kg) naringin before single CYCP (200 mg/kg, i.p.) administration. Afterwards, the rats were sacrificed. Naringin concentrations required for 50 % scavenging hydrogen peroxide and nitric oxide radical were 0.27 mg/mL and 0.28 mg/mL, respectively. Naringin pretreatment significantly (p < 0.05) protected erythrocytes plasma membrane architecture and integrity by abolishing CYCP-induced decrease in the activity of erythrocyte LDH (a marker of ATP). Pretreatment with naringin remarkably (p < 0.05) reversed CYCP-induced decreases in the erythrocytes glutathione levels, activities of glutathione-S-transferase, catalase, glutathione peroxidase, and glutathione reductase; attenuated CYCP-mediated increases in erythrocytes levels of malondialdehyde, nitric oxide, and major lipids (cholesterol, triacylglycerol, phospholipids, and non-esterified fatty acids). Taken together, different acute pretreatment doses of naringin might avert CYCP-mediated erythrocytes dysfunctions via its antioxidant, free-radical scavenging, and anti-dyslipidaemia properties.

Camphor-induced oxidative stress and histopathological changes (in brain, lung, liver, kidney and testes) have been reported. We therefore investigated the effect of various doses of camphor in an acute study, on renal and testicular levels of some pro-inflammatory mediators in male wistar rats. Twenty rats divided into four groups of five rats each were used in this study. Group 1 served as control and was administered 6 mL/kg olive oil, the vehicle for camphor, while groups 2, 3 and 4 were orally administered 1000, 2000, and 4000 mg/kg body weight camphor, for seven days. Compared with control, levels of tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β) and interleukin 6 (IL-6) were significantly increased kidney and testes by 2000 and 4000 mg/kg body weight, while interleukin 10 (IL-10) was only significantly increased by 1000 mg/kg body weight of camphor in both tissues. Also compared with control, all doses of camphor administered resulted in a significant increase in the expressions of renal and testicular nuclear factor kappa B (NFkB), cyclooxygenase 2 (COX-2), regulated upon activation normal T cell expressed and secreted (RANTES), and monocyte chemo-attractant protein 1 (MCP-1). Conclusively, use and consumption of camphor should be with caution as it could trigger renal and testicular inflammation through activation of NF-kB and up-regulation of pro-inflammatory markers. Keywords: Camphor, Chemokines, Cytokines, Pro-inflammation, Renal, Testicular