Antioxidant capacity of N-acetylcysteine against the molecular and cytotoxic implications of cadmium chloride leading to hepatotoxicity and vital progression.

Many studies have reported that cadmium (Cd) can induce liver cell injury; however, the toxicity mechanisms of Cd on the liver have not been fully explained. Thirty-two male albino rats were divided into four groups: the control group, the N-acetylcysteine (NAC) group orally as effervescent instant sachets with a concentration of 200 mg dissolved in distilled water and dosage was 200 mg/kg body weight freshly prepared, the cadmium chloride (CdCl) group (treated with 3 mg/kg orally), and the N-acetylcysteine (NAC) + cadmium chloride group (treated with 200 mg/kg orally post to CdCl) for 60 days. The NAC alone did not make notable changes in most of the parameters.

Role of let7-g and miR-221 level as potential predictors for overall survival of hepatocellular carcinoma patients.

Background And Study Aims: Hepatocellular carcinoma (HCC) is one of the most common cancer types worldwide. A hallmark of epithelial-mesenchymal transition is the loss of epithelial E-cadherin, which is considered an epithelial differentiation marker. MicroRNAs serve vital roles in various biological processes in the cell via post-transcriptional gene regulation.

N-Acetylcysteine Reduces miR-146a and NF-κB p65 Inflammatory Signaling Following Cadmium Hepatotoxicity in Rats.

We performed a thorough screening and analysis of the impact of cadmium chloride (CdCl) and N-acetylcysteine (NAC) on the miR146a/NF-κB p65 inflammatory pathway and mitochondrial biogenesis dysfunction in male albino rats. A total of 24 male albino rats were divided into three groups: a control group, a CdCl-treated group (3 mg/kg, orally), and a CdCl + NAC-treated group (200 mg/kg of NAC, 1 h after CdCl treatment), for 60 consecutive days. Real-time quantitative PCR was used to analyze the expression of miR146a, Irak1, Traf6, Nrf1, Nfe2l2, Pparg, Prkaa, Stat3, Tfam, Tnfa, and Il1b, whereas tumor necrosis factor-α, interleukin-1β, and cyclooxygenase-2 protein levels were assessed using ELISA, and NF-κB p65 was detected using western blotting.

Protocatechuic acid mitigates cadmium-induced neurotoxicity in rats: Role of oxidative stress, inflammation and apoptosis.

Environmental and occupational exposure to heavy metals, including cadmium (Cd), is associated with extremely adverse impacts to living systems. Antioxidant agents are suggested to eliminate Cd intoxication. In this paper, we investigated the potential neuroprotective effect of protocatechuic acid (PCA) against Cd-induced neuronal damage in rats.

Exposure to arsenite and cadmium induces organotoxicity and miRNAs deregulation in male rats.

Sodium arsenite (NaAsO) and cadmium chloride (CdCl) are two prime examples of un-biodegradable compounds that accumulate in the ecosystems causing great threats to human health and produce severe adverse effects. However, their joint toxicities are poorly understood in mammals. This study aimed to identify the effect of exposure to NaAsO (5 mg/kg, by oral gavage) and CdCl (1 mg/kg injected interperitoneal, i.