Acrolein Group Research Articles

Whey protein protects liver mitochondrial function against oxidative stress in rats exposed to acrolein.

Acrolein (AC) is one of the most toxic environmental pollutants, often associated with incomplete combustion of petrol, wood, and plastic, oil frying, and tobacco smoking, that causes oxidative damage to DNA and mitochondria. Considering that little is known about the protective effects of whey protein (WP) against AC-induced liver toxicity, the aim of our study was to learn more about them in respect to liver mitochondrial oxidative stress, respiratory enzymes, Krebs cycle enzymes, and adenosine triphosphate (ATP). To do that, we treated Sprague Dawley rats with daily doses of AC alone (5 mg/kg bw in 0.9 % NaCl solution), WP alone (200 mg/kg bw, in 0.9 % NaCl solution), or their combination by oral gavage for six days a week over 30 days. As expected, the AC group showed a drop in glutathione levels and antioxidant, transport chain, and tricarboxylic acid cycle enzyme activities and a significant rise in mitochondrial lipid peroxidation and protein carbonyl levels. Co-treatment with WP mitigated oxidative stress and improved enzyme activities. Judging by the measured parameters, WP reduced AC toxicity by improving bioenergetic mechanisms and eliminating oxidative stress.

Protective effect of lutein against acrolein-induced ototoxicity in rats

BackgroundAcrolein is a reactive aldehyde that forms during burning of wood and other fuels. It is also a product of lipid peroxidation (LPO) reactions and is present in cigarette smoke. Acrolein is known to cause oxidative stress and inflammatory nerve tissue damage. Lutein is a tetraterpenoid molecule with antioxidant and anti-inflammatory properties. There appear to be no studies on the effect of lutein on vestibulocochlear nerve damage induced by acrolein. The aim of this study was to investigate the effect of lutein on vestibulocochlear nerve damage induced by acrolein in rats using biochemical and histopathological methods. MethodsThe rats were divided into three groups (n = 6, for each group) a healthy control group (HG), an acrolein (ACR) group and a lutein and acrolein (LACR) group. In the LACR group, lutein was administered (1 mg/kg) via oral gavage. The ACR and HG groups received saline via oral gavage. Then, 1 h after the administration of lutein and saline, the LACR and ACR groups were treated with 3 mg/kg of acrolein via oral gavage. This procedure was repeated once a day for 30 days. ResultsThe results of biochemical experiments showed that in the vestibulocochlear nerve tissues of the animals treated with acrolein, the levels of malondialdehyde, total oxidants, nuclear factor kappa b, tumor necrosis factor alpha and interleukin 1 beta significantly increased, whereas the levels of total glutathione and total antioxidants decreased as compared to those in the HG and LACR groups. In addition, severe histopathological damage was observed in vestibulocochlear nerve tissue of the acrolein group, whereas this damage was alleviated in the lutein group. ConclusionLutein protected vestibulocochlear nerve tissue from acrolein-associated oxidative and proinflammatory damage. This suggests that lutein might be useful in preventing or treating acrolein-induced ototoxicity.

Ameliorative Effect of Pentoxifylline a Phosphodiesterase-5 on Acrolein Induced Oxidative ‎Damage

Background:: Pentoxifylline (PTX), a methylxanthine derivative and nonspecific type 5 phosphodiesterase (PDE) inhibitor, is a drug widely used in the management of peripheral arterial disease. Objectives:: The aim of this study was to investigate the possible protective role of PTX on toxicity of acrolein (ACR). Materials and Methods:: In this experimental study, 30 male rats were equally divided in to 6 groups (5 rats each). ‎Group I (control) that received normal saline, group II was given ACR (2 mg /kg/day, i.p.). Animals of group ‎III received only PTX (50 mg/kg/day, i.p.). Group IV was given ACR + PTX, groups V received only vitamin E (15 mg/kg/day, s.c.) and group VI was given vitamin E combination to ACR once ‎daily for 14 dayes. Oxidative damage were measured by oxidative biomarkers such as glutathione peroxidase (GPx), superoxide dismutase (SOD), lipid peroxidation (LPO) and total glutathione (GSH) in blood of rats. Results:: At the end of the experiment, the plasma of the animals was separated. In the blood plasma, ACR reduced total glutathione (GSH), SOD and GPx compared control group. Also, the LPO was increased in the ACR group as compared with controls. PTX ameliorated LPO, SOD and GPx in blood of ACR-induced changes. Conclusions:: These findings suggest that PTX ‎may provide a promising approach for the treatment of ACR-related diseases throughout reduction oxidative injuries.