Carnosic acid attenuates acrylamide-induced retinal toxicity in zebrafish embryos

Abstract

Acrylamide (ACR) is a water-soluble chemical used widely in industry, which can be formed in tobacco smoke and in starchy foods cooked at high temperatures. ACR is considered to be a neurotoxin, genotoxin and carcinotoxin. Previous studies reported that ACR-exposed workers and experimental animals exhibited visual function defects, although the underlying mechanisms have not been elucidated. In this study, we found that zebrafish embryos exposed to 1 mM and 2 mM ACR showed significantly increased reactive oxygen species (ROS), decreased expression of the antioxidant genes Sod1, Sod2, Catalase, Gpx1 and Nrf2, reduced activity of superoxide dismutase (SOD) and catalase, and elevated malondialdehyde (MDA), compared with control embryos. ACR exposure caused loss of both rod and cone photoreceptor cells through Caspase-3-dependent apoptotis. When embryos were simultaneously exposed to ACR and the natural antioxidative substance carnosic acid (CA), the presence of the latter (10 μM) markedly counteracted the above ACR-induced toxic effects. Our data suggest that CA can protect photoreceptor cells against ACR-induced oxidative damage and has a potential for neuroprotection of visual function in humans exposed to ACR.

Protective effect of carnosic acid on acrylamide‐induced liver toxicity in rats: Mechanistic approach over Nrf2‐Keap1 pathway

“…This discrepancy might stem from different experimental duration and substance dose regimen as well as the interplay between the toxic and the protective substances. In a study of Albalawi et al [ 36 ] in zebrafish embryos, carnosic acid reduced acrylamide‐induced retinal toxicity. In addition, in contrast to our results, they found that while acrylamide alone decreased Nrf2 levels, carnosic acid cotreated with acrylamide increased Nrf2 levels.…”

Preventive Effects of Three Polysaccharides on the Oxidative Stress Induced by Acrylamide in a Saccharomyces cerevisiae Model

“…The effect of AA on SOD activity in different experimental models has been reported in many previous studies, but the results seem to be inconsistent. The observation result of some studies is that under the administration of AA, SOD enzyme activity was significantly inhibited, which indicates that AA induced redox imbalance and the antioxidant defense system failed to combat the influx of ROS [ 31 , 40 , 41 , 42 ]. In contrast, another part of the study showed that the stimulation of AA increased the activity of SOD, and it is thought to be a compensatory mechanism against oxidative stress [ 3 , 20 , 43 ].…”

Untitled

“…Extensive studies in rodents and other experimental models have demonstrated that exposure to monomeric ACR to cause carcinogenicity, developmental toxicity, neurotoxicity, and genotoxicity 2 .…”