An assessment of the ameliorative role of hesperidin in Drosophila melanogaster model of cadmium chloride-induced toxicity.

Cadmium chloride (CdCl2) is an important heavy metal widely regarded as an environmental contaminant. Hesperidin, a flavanone glycoside found in citrus fruits, has an established properties against free radicals, apoptosis, and inflammation. The present study investigated the protective actions of hesperidin on CdCl2-induced oxidative damage and inflammation in Drosophila melanogaster. For 7 consecutive days via their diet regimen, the flies were exposed to CdCl2 alone (0.05 mM) or in combination with hesperidin (50 and 100 µM). Exposure to CdCl2 significantly (p < 0.05) increased mortality rate of flies, whereas the survived flies demonstrated significant oxidative toxicity from decreased activities of catalase and Glutathione S-transferase (GST) and Total Thiol (T-SH) and Non-Protein Thiols (NPSH) levels as well as accumulation of Nitric Oxide (NO (nitrite/nitrate)), protein carbonyl and Hydrogen Peroxide (H2O2). However, hesperidin-supplemented diet improved Acetylcholinesterase (AChE) activity, mitochondrial metabolic rate (cell viability), locomotor activity, and amelioration of oxidative damage and lipid peroxidation induced by CdCl2. The hesperidin diet supplement boosted the antioxidant milieu and ameliorated the oxidative damage in the treated flies. Overall, the findings revealed that hesperidin improved antioxidative protective capacity in Drosophila melanogaster model of CdCl2-induced toxicity. This suggests hesperidin as a potential therapeutic agent against oxidative stress disorders due to exposure to CdCl2 and or related toxicants.

Protocatechuic acid modulates hepatic oxidative stress and inflammation linked to DMN exposure in rat.

Dimethyl nitrosamine (DMN), a potent hepatotoxin, exerts carcinogenic effects and induces hepatic necrosis in experimental animals via CYP2E1 metabolic activation, and generation of reactive oxygen species (ROS). Protocatechuic acid (PCA), a plant-based simple phenolic compound and potent antioxidant, has been shown to affect the development of neoplasia in the rat liver and inhibit the initiation or progression phases of most cancers. In this study, the modulatory effects of PCA on DMN-induced hepatotoxicity, oxidative stress, inflammation, and selected phase I xenobiotic metabolizing enzymes were investigated in male Wistar rats. This study assessed biomarkers of hepatic injury (alanine transaminase, aspartate aminotransferase, alkaline phosphatase, and gamma- glutamyl transferase); oxidative stress (hydrogen peroxide concentration, lipid peroxidation, and reduced glutathione levels); measured activities of antioxidant enzymes (catalase, sodium dismutase, glutathione peroxidase, glutathione S-transferase); and inflammation (Tumor necrosis factor (TNF)-α, interleukin-1-Beta (IL-1ß) and iNOS). The results of our investigation demonstrated that pretreatment with PCA at 50 and 100 mg/kg body weight p.o. reduced DMN (20 mg/kg bw) i.p. mediated hepatic injury, oxidative stress, and inflammation in a dose-dependent manner. In addition, the activities of phase I metabolizing enzymes were significantly induced except for aminopyrine-N-demethylase in the DMN-treated rats when compared with the DMN alone control group. This induction was also reversed by pre-treatment with PCA. The result of this study suggests that PCA is hepatoprotective against DMN-induced hepatic damage by its ability to suppress oxidative stress, inflammation, and modulate the activities of the selected phase I drug metabolizing enzymes. Thus, PCA may prove useful in combating DMN-induced hepatic damage.

Sodium benzoate induces neurobehavioral deficits and brain oxido-inflammatory stress in male Wistar rats: Ameliorative role of ascorbic acid.

BACKGROUND: Sodium benzoate (SB) is a widely used food preservative. However, excessive intake of a high dose of SB poses a risk of neurotoxicity. Ascorbic acid (AA) is a naturally occurring antioxidant found in fruits with reported neuroprotective properties. The present study investigated the neurobehavioral and biochemical alterations in SB-treated rats and the ameliorative effect of AA in rats. METHODS: Forty-two male Wistar rats were divided into six groups (n = 7). Group 1 (vehicle, 10 ml/kg), Groups 2-4 rats SB (150, 300, and 600 mg/kg), Group 5 AA (100 mg/kg) and Group 6 (SB 600 mg/kg + AA 100 mg/kg). Treatment was daily administered for 28 days by oral route. Anxiogenic behavior, locomotor, and exploratory activities were evaluated in the open field monitored with a camera, and memory performance in Y-maze. Brain oxidative stress, inflammatory, apoptosis, and cholinergic markers were determined. The cortico-hippocampal tissues were examined histologically. RESULTS: SB-treated rats showed significant anxiogenic-like behavior and impairment in locomotor, exploratory, and memory performance. This was reversed in SB (600 mg/kg)-treated rats coadministered with AA. SB-treated rats showed a decrease in antioxidant enzyme activities, increase malondialdehyde (MDA), nitrite, tumor necrosis factor-alpha, caspase-3, and acetylcholinesterase activity in the striatum, hippocampus, frontal cortex, and cerebellum. These biochemical changes were reversed in AA-treated rats. Reduced cortico-hippocampal neuronal cell count and the pyknotic index were found in SB-treated rats, which was also reversed in AA-treated rats. CONCLUSION: Conclusively, sodium-benzoate-induced neurobehavioral deficits and brain biochemical changes were ameliorated by ascorbic acid probably via antioxidant, anti-inflammatory, and apoptotic mechanisms.

Occurrence of BTEX from petroleum hydrocarbons in surface water, sediment, and biota from Ubeji Creek of Delta State, Nigeria.

Petroleum exploration and production activities pose great threat worldwide in the marine environment with numerous occurrences of spills every year. Ubeji Creek in Nigeria suffers environmental pollution attributable to petroleum exploration. The hydrocarbons in petroleum encompass a large number of toxicants such as BTEX, which are frequently discharged into water bodies during spillage. In terms of scope, this study assessed for the first time BTEX levels in surface water, sediment, and biota of the Ubeji Creek. Environmental samples were collected at designated sampling locations along the Ubeji Creek quarterly for 2 years. Water quality was determined in situ, while BTEX levels in water, sediment, and biota were assessed in the laboratory using GC-FID. The physico-chemical characteristics of water were within the acceptable WHO limits with the exception of DO of 3.01 ± 0.25 mg/L. Organic pollution load could have contributed to the depression of DO level below the limit. BTEX of 5.57 ± 0.62 mg/kg in sediment samples was higher than the level in control sample. The BTEX levels in fish, shrimps, pawpaw fruit, pineapple tissue, bitter leaf, and cassava were 0.37 ± 0.05, 0.39 ± 0.01, 0.56 ± 0.02, 1.35 ± 0.04, 0.46 ± 0.06, and 0.22 ± 0.01 mg/kg, respectively. Accumulation of BTEX in this biota can affect their nutritive quality and consequently pose threat to humans who daily consume them.