Ameliorative potential of eriocitrin against cadmium instigated hepatotoxicity in rats via regulating Nrf2/keap1 pathway.

BACKGROUND: Cadmium (Cd) is a hazardous heavy metal that adversely affects the vital body organs particularly liver. Eriocitrin (ERCN) is a plant-based flavonoid that is well-known for its wide range of pharmacological potential. This research trial was aimed to determine the ameliorative potential of ERCN against Cd provoked hepatotoxicity in rats. METHODOLOGY: Twenty-four rats (Rattus norvegicus) were apportioned into control, Cd treated (5 mg/kg), Cd (5 mg/kg) + ERCN (25 mg/kg) and only ERCN (25 mg/kg) administrated group. Expressions of Nrf2/Keap1 pathway and apoptotic markers were assessed through qRT-PCR. The levels of inflammatory and liver function markers were evaluated by using standard ELISA kits. KEY FINDINGS: Cd exposure reduced the expression of Nrf2 and anti-oxidant genes as well as the activity of catalase (CAT), glutathione reductase (GSR), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST) and glutathione (GSH) contents while escalating the expression of Keap1. Furthermore, Cd intoxication augmented malondialdehyde (MDA) and reactive oxygen species (ROS) levels in hepatic tissues. Exposure to Cd resulted in a notable elevation in the levels of alanine transaminase (ALT), alkaline phosphatase (ALP) and aspartate aminotransferase (AST). Cd administration upregulated nuclear factor-kappa B (NF-κB), interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) levels as well as cyclooxygenase-2 (COX-2) activity. Furthermore, Cd administration upsurged Bax and Caspase-3 expression while reducing the expression of Bcl-2. Moreover, Cd intoxication disrupted the normal architecture of hepatic tissues. However, supplementation of ERCN significantly (p < 0.05) ameliorated the aforementioned disruptions induced by Cd intoxication. CONCLUSION: ERCN treatment remarkably ameliorated the hepatic tissues owing to its antioxidant, anti-inflammatory, and anti-apoptotic potentials. These findings underscore the therapeutic potential of ERCN to counteract the adverse effects of environmental pollutants on hepatic tissues.

Protective effects of vitexin on cadmium-induced renal toxicity in rats.

Cadmium (Cd) is an industrial contaminant that poses severe threats to human and animal health. Vitexin (VIT) is a polyphenolic flavonoid of characteristic pharmacological properties. We explored the curative role of vitexin on Cd-induced mitochondrial-dysfunction in rat renal tissues. Twenty-four rats were equally divided into four groups and designated as control, Cd, Cd + vitexin and vitexin treated groups. The results showed that Cd exposure increased urea and creatinine levels while decreased creatinine clearance. Cd reduced the activities of antioxidant enzymes, i.e., catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione content in the Cd exposed group. Cd exposure significantly (p < 0.05) elevated the reactive oxygen species (ROS) and Thiobarbituric acid reactive substances (TBARS) levels in rat kidney. Cd also caused a significant (p < 0.05) reduction in the mitochondrial TCA-cycle enzymes, including isocitrate dehydrogenase, succinate dehydrogenase, alpha-ketoglutarate dehydrogenase, and malate-dehydrogenase activities. Besides, mitochondrial respiratory chain enzymes, including NADH-dehydrogenase, coenzyme Q-cytochrome reductase, succinic-coenzyme Q, and cytochrome c-oxidase activities were also decreased under Cd exposure. Cd exposure also damaged the mitochondrial membrane potential (MMP). However, VIT treatment potentially reduced the detrimental effects of Cd in the kidney of rats. In conclusion, our study indicated that the VIT could attenuate the Cd-induced renal toxicity in rats.

A study on the potential reprotoxic effects of thimerosal in male albino rats.

Thimerosal is ethyl mercury based compound which is being used as a preservative in vaccines since decades. Pharmaceutical products and vaccines that contain thimerosal are among the potential source of mercury exposure. Current research was intended to ascertain the reprotoxic effects of thimerosal on rat testes. Twenty-four adult male albino rats were sorted into four groups (n = 6). The first group was a control group. Rats of experimental Group 2, 3 and 4 were treated with various dosages of thimerosal (0.5, 10, 50 mg/kg) respectively. Rats were decapitated after thirty days of trial and different parameters were analyzed. Thimerosal exposure resulted in a significant decrease in antioxidant enzyme activities including catalase (CAT), peroxidase (POD), superoxide dismutase (SOD), glutathione reductase (GSR) and increased levels of thiobarbituric acid reactive substances (TBARS). Different doses of thimerosal significantly decreased (p < 0.05) the concentration of plasma testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH). Additionally, Daily sperm production (DSP) and efficiency of daily sperm production were significantly reduced followed by thimerosal exposure. Moreover, thimerosal significantly (p < 0.05) decreased the primary spermatocytes, secondary spermatocytes, number of spermatogonia along with spermatids. Thimerosal induced adverse histopathological and morphological changes in testicular tissues such as decreased Leydig cells, diameter of seminiferous tubules, tunica albuginea height and epithelial height. On the other hand, the increase in tubular lumen and interstitial spaces was observed due to thimerosal. These outcomes indicated that thimerosal has potential reprotoxic effects in male albino rats.