d-Amphetamine-induced cytotoxicity and oxidative stress in isolated rat hepatocytes

Genotoxic effects induced by the exposure to an environmental mixture of illicit drugs to the zebra mussel

“…Since our previous study of zebra mussel specimens exposed for 14 days to the same illicit drug mixture showed a significant activation of antioxidant defenses, as well as significant increase of protein carbonylation , we can suppose that the tested mixture can promote the ROS overproduction and be partially or totally responsible for genotoxicity found in zebra mussel treated specimens. In addition, our data were supported by many studies of murine models showing that both in vitro and in vivo exposure to COC and all its metabolites, including BE (Neri et al, 2013 and reference therein), AMPH (Cadet et al, 2007;El-Tawil et al, 2011), MDMA (Alvarenga et al, 2010) and MOR (Zhang et al, 2004) promoted ROS overproduction, which was recognized as a crucial factor inducing diverse genetic injuries to cells from different organs after the treatment with high concentrations of each single drug. The correlation analysis among the data from genotoxicity biomarkers and oxidative stress endpoints from our previous study showed that the LDR, the percentage of DNA in the comet tail and the frequency of apoptotic cells were positively and significantly (p o0.05) correlated with all the antioxidant enzyme activities (with the exception of percentage of DNA in the comet tail and SOD activity; Table 1).…”

Kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo

“…LDH and AST are relatively stable enzymes in BRL cells, thus their leakage from the intracellular compartment of hepatocytes into the extracellular space indicates that plasma membrane disruption and hepatocyte damage have occurred. 32,33 In this study, the elevated levels of these enzymes in the supernatants of BRL cells may be correlated with the increased release of ROS, TNF-α, and NO by activated KCs, as previously mentioned. Studies have demonstrated that ROS are capable of causing oxidative damage to major cellular structures, in particular the …”

Oxidative Stress and ADHD

“…Although dopamine and other catecholamines possess antioxidative and free radical scavenging properties (Cao, Sofic, & Prior, 1997; Yen & Hsieh, 1997), dopamine is easily oxidized and generates highly reactive metabolites such as dopamine quinone, which further lead to mitochondrial dysfunction and oxidative stress (Miyazaki & Asanuma, 2008). Thus, it is not surprising to see the “paradoxical effect” of stimulant treatment, which causes oxidative stress (El-Tawil, Abou-Hadeed, El-Bab, & Shalaby, 2011; Martins et al, 2006) but is also neuroprotective (Volz, 2008) and is an effective treatment for ADHD (Faraone & Buitelaar, 2010). In contrast, clonidine, which is also an effective treatment for ADHD, reduces oxidative stress in rats (Filos et al, 2012; Nik Yusoff, Mustapha, Govindasamy, & Sirajudeen, 2013).…”