Shaktitaur Oxidative Medicine and Cellular Longevity Serum and tissue lycopene and biomarkers of oxidation in prostate cancer patients: Furthermore, even at low oxygen tension, it can also scavenge peroxyl radicals, lycoprne the process of lipid peroxidation[ 11 ]. Sachdeva AK, Chopra K. Abdel-Rahman1 Heba M. Lycopene LYC is a natural antioxidant and free radical scavenger lipophilic carotenoid present in food especially tomatoes giving it the red color [ 17 ].
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Control and LYC groups show week immunoreactivity of caspase-3 while BPA-treated group exhibited higher immunoreactivity. Discussion BPA is a monomer found in plastic goods and affects adversely many organs especially the liver through induction of oxidation state.
The present results demonstrated that BPA had no effect on body and liver weights. However, B. G to a level comparable to control. These results could be attributed to the toxic effect of BPA that could encounter several body homeostatic pathways, among which neuronal appetite loop in the brain [ 38 ], where BPA can easily cross blood brain barrier and have estrogenic effect [ 39 ]. Moreover, BPA can alter the antioxidant enzymes in different body systems [ 40 , 41 ] as noted in the current study, thus could alter normal weight gain of the experimental rats.
This can obviously illustrate the higher B. Our results were in harmony with Morrissey et al. G in BPA-treated female mice offspring and insignificant change in F.
On the other hand, some reports in the literatures were inconsistent to our findings, where Rubin et al. The variation in results may be attributed to the diversity in diet composition, BPA exposure period, route and doses, and animal strain. In our data, BPA expressed harmful effect on the liver evidenced by significant increase in the serum liver enzyme activities along with reduction in TP and albumin. This is augmented by the observed depletion in the activities of endogenous enzymatic antioxidants SOD, GPx, and CYPR that could increase hepatic membrane lipid peroxidation that disrupt its permeability [ 48 ].
Meanwhile, serum protein concentration is considered equilibrium between the rate of protein synthesis and breakdown. It is well known that BPA induces mitochondrial oxidative stress in the cell that results in protein damage [ 49 ], thus making protein damage more prominent than its synthesis. Moreover, administration of BPA disrupted hepatic integrity and functions where liver is considered the main organ involved in plasma protein biosynthesis [ 50 ]; thus, serum TP and albumin were declined.
These obtained results were concurring with those recorded by Moon et al. This finding harmonized with Sheriff and Devaki [ 54 ] and Jiang et al. Consequently, it strengthens the cellular membrane while diminishing the enzyme leakage and preserves its function in protein biosynthesis. Administration of BPA in current study disrupted lipid metabolism that reflected negatively on serum profile results. Our results were in agreement with Moghaddam et al.
BPA has the capability to disrupt the lipid metabolism [ 56 ] and trigger lipid accumulation through differentiation of 3T3-L1 fibroblasts into adipocytes [ 57 ]. The occurrence of abnormalities in lipid profile is considered the starting station for induction of oxidative stress and lipid peroxidation [ 58 ] that were observed in the current study. Jiang et al. These results were in harmony with those obtained by Kabuto et al.
The reduction in serum SOD activity could be due to excessive consumption in the autoxidation procedure induced by BPA in the liver.
The decrease in SOD activity might lead to increase level of superoxide radicals which resulted in the inactivation of GPx [ 63 ], thus increasing hydrogen peroxide generation [ 11 ]. The antioxidant activity of LYC could be attributed to being a beta carotene, where LYC had been proved to protect against protein, lipid, and DNA oxidation [ 67 ] through scavenging singlet oxygen [ 68 ] and peroxyl radicals [ 69 ], thus limiting MDA production as lipid peroxidation end product [ 70 ].
These results were similar to those obtained by Eid et al. Current histopathological picture was confirmative for the oxidative stress and lipid peroxidation induction nature of BPA observed in this study. The usage of LYC, as antioxidant, produced pronounced hepatic protection that markedly ameliorated the severity of hepatic lesions and subsequently the hepatic functions. Hepatic homeostasis is gained through a regular cell turnover involving apoptosis of hepatocytes [ 71 ]. The increase of apoptosis via increment of DNA strand breaks with DNA migration from the nucleus into the comet tail together with increment in caspase-3 protein content in BPA group is an attribution for various types of the observed liver pathology.
Current results were parallel to the previous results of Abdel Samie et al. Our data suggested that BPA increased caspase-3 apoptosis and DNA tail fragment breaks via depletion of antioxidant activities and lipid peroxidation. These results were in agreement with Kurcer et al. The possible attribution for LYC antiapoptotic effect is its antioxidant power as it is known for its free radical scavenging effect that reduces lipid peroxidation, protein, and DNA damage [ 74 , 75 ]. All these effects downregulated hepatic caspase-3, thus reducing apoptosis and thus keeping hepatic integrity, and prevented the liberation of hepatic enzymes into the blood of female Wistar rats.
Conflicts of Interest All authors have no competing interests to state. Acknowledgments Eternal thanks to Prof. Amina El Dessouki, Department of Pathology, for giving histopathology comments. References D. Wu and A. View at: Google Scholar D. Reische, D. Lillard, and R. View at: Google Scholar S.
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LYCOPENE HEPATOPROTECTIVE PDF
M Anusha, E-mail: moc. This article has been cited by other articles in PMC. Abstract Objective: To investigate the hepatoprotective activity of the aqueous extract of the aerial parts of Portulaca oleracea P. Materials and Methods: Hepatotoxicity was induced in male Wistar rats by intraperitoneal injection of carbon tetrachloride 0. The aqueous extract of P. The hepatoprotective activity of the combination was evaluated by the liver function marker enzymes in the serum [aspartate transaminases AST , alanine transaminases ALT , alkaline phosphatase Alk. Results: Both the treatment groups showed hepatoprotective effect against carbon tetrachloride induced hepatotoxicity by significantly restoring the levels of serum enzymes to normal which was comparable to that of silymarin group.
Hepatoprotective and antioxidant effects of lycopene in acute cholestasis.