Protective Effect Of Lycopene Research Articles

The role of lycopene in alleviating nanoplastic-induced liver inflammation and steatosis: Insights from gut microbiota remodeling

Nanoplastics (NPs) are emerging pollutants that are widespread in food and drinking water and present a serious danger to the health of animals and humans. Therefore, it is increasingly important to dissect their targeted toxicity mechanism and explore how to mitigate their damaging effects on the organism. Lycopene (LYC)possesses anti-inflammatory, antioxidant, and lipid metabolism– and intestinal microbiota–regulating properties. The research sought to assess the defensive properties of LYC in preventing liver lipid metabolism disorder in mice induced by chronic exposure to nanoparticles. The results indicated that LYC treatment significantly decreased the accumulation of tissue NPs, promoted the excretion of fecal NPs, remodeled intestinal flora, alleviated intestinal injury, decreased circulating lipopolysaccharide production, inhibited the liver TLR4/NF-κB pathway, and ultimately attenuated NPs-induced liver inflammation and steatosis in mice. Interestingly, ablation of the gut microbiota by antibiotic treatment reversed, to some extent, the protective effects of LYC on the NPs-induced disturbances in liver function and lipid metabolism. The fecal transplantation experiment showed that the mice transplanted with microbiota from the NPs + LYC mice had similar phenotypes to those of donor mice, including alleviated liver injury and lipid metabolism disorder. In conclusion, LYC treatment ameliorates liver damage and lipid metabolism disorder caused by NPs, possibly through the modulation of the gut microbiota/liver TLR4/NF-κB signaling axis. This supports LYC as a potential dietary therapy for treating liver steatosis caused by NPs.

Amelioration of Atherosclerosis by lycopene is linked to the modulation of gut microbiota dysbiosis and related gut-heart axis activation in high-fat diet-fed ApoE−/− mice

BackgroundInterplay between gut microbiota and heart, termed “gut-heart” axis, has a crucial role in the pathogenesis of atherosclerosis. Our previous study showed that lycopene possesses anti-inflammatory and anti-atherosclerotic effects, but its link to the gut microbiota is poorly understood. Herein, we surmised that lycopene could regulate the gut microbiota, exert anti-atherosclerotic effect by regulating the “gut-heart” axis.MethodsMale ApoE−/− mice were fed a high-fat diet (HFD) with or without lycopene (0.1% w/w) for 19 weeks. Gut microbiota was analyzed by 16 S rRNA sequencing, the protein levels of zonula occludens-1 (ZO-1), occludin, toll-like receptor 4 (TLR4) and phospho-nuclear factor-κB (NF-κB) p65 were measured by Western blotting, the levels of serum inflammatory factors including monocyte chemotactic protein 1 (MCP-1), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 were assayed using ELISA kits. Also, the concentrations of serum lipopolysaccharide (LPS), D-lactic acid (D-LA) and diamine peroxidase (DAO) were measured through ELISA method.ResultsThe aortic sinus sections revealed that lycopene supplementation significantly reduced the extent of atherosclerotic lesions and inhibited atherosclerosis development caused by HFD. The analysis of gut microbiota showed that lycopene reduced the ratio of Firmicutes/Bacteroides and increased the relative abundance of Verrucomicrobia, Akkermansia and Alloprevotella, which were related to elevated intestinal barrier function and reduced inflammation. Moreover, lycopene up-regulated the expression of intestinal ZO-1 and occludin and decreased serum LPS, D-LA and DAO levels. In addition, lycopene inhibited the expression of TLR4 and phospho-NF-κB p65 in aortic sinus plaque, serum MCP-1, TNF-α, IL-1β, and IL-6 levels were also lowered by lycopene treatment.ConclusionsOur results indicated the protective effect of lycopene against atherosclerosis induced by HFD and further revealed that its mechanism might be its prebiotic effect on maintaining gut microbiota homeostasis and improving intestinal barrier function, consequently reducing serum LPS-triggered inflammatory response in the heart.

Lycopene protects against ionizing radiation-induced testicular damage by inhibition of apoptosis and mitochondrial dysfunction.

Ionizing radiation (IR) is one of the key contributors that cause male infertility by disturbing spermatogenesis. Lycopene, a carotenoid with strong antioxidant properties, was shown to protect against oxidative damage induced by IR in several experimental models. The present study was designed to explore the possible protective effects of lycopene against IR-induced testicular damage in C57BL/6 mice. Mice were administered lycopene (20 mg/kg) by oral gavage for seven consecutive days prior to a single dose of whole-body X-ray irradiation (4 Gy, 1 Gy/min). We observed that lycopene remarkably augmented sperm motility and reduced sperm abnormalities in mice following IR exposure. Histopathological analyses also revealed that lycopene ameliorated the structural damage of seminiferous tubules and enhanced the regeneration of seminiferous epithelium following IR stress. Moreover, lycopene attenuated IR-induced oxidative stress, as evidenced by a decreasing lipid peroxidation level and an increase in the antioxidant enzyme superoxide dismutase activity. In addition, lycopene reduced the γH2AX expression and the number of TUNEL-positive cells in the germinal epithelium, as well as restoring the imbalance of Bax/Bcl-2 expression induced by IR exposure. Furthermore, lycopene prevented mitochondrial membrane potential depolarization and ATP reduction and preserved the activities of mitochondrial complexes I-IV in the testes of mice after exposure to IR. Lycopene also improved mitochondrial biogenesis in testes of mice exposed to IR, presenting as restored expressions of PGC-1α, Nrf1, and Tfam. Taken together, our results suggest that lycopene alleviates IR-induced testicular damage, and the underlying mechanism involves at least in part the inhibition of the mitochondrial apoptotic pathway and the maintenance of mitochondrial respiration and biogenesis. The beneficial effect of lycopene highlights the therapeutic potential of this plant-derived antioxidant against impaired spermatogenesis and male infertility induced by IR.

The possible ameliorative role of Lycopene on Tributyltin induced thyroid damage in adult male albino rats (histological, immunohistochemical and biochemical study)

ABSTRACT Tributyltin is used in industrial applications. This current research aimed to study the effect of Tributyltin on the thyroid gland structure and function of adult male albino rats and the protective effect of Lycopene. Twenty-one male adult albino rats were classified into three groups: Control, treated that received Tributyltin, and protective that received Lycopene with Tributyltin. At the end of the experiment, blood samples were collected and T4, T3, and (TSH) were measured. Tissue superoxide dismutase (SOD) and malondialdehyde (MDA) were estimated. Thyroid gland specimens were processed for histological and immunohistochemical examination. Then morphometric and statistical analyses were done. The treated group showed affection in thyroid function and histological structure as vacuolated colloid and cytoplasm and dark nuclei. Ultrastructurally, follicular cells showed irregular shrunken nuclei, atrophied apical microvilli, vacuoles, multiple lysosomal granules, mitochondria with destructed cristae, and extensively dilated rough endoplasmic reticulum. There was increase in Caspase-3 immunoexpression and decrease in Beclin-1 immunoexpression. The thyroid structure and biochemical markers improved after Lycopene administration. The thyroid gland damage caused by Tributyltin is ameliorated by Lycopene.

Lycopene prevents Di-(2-ethylhexyl) phthalate-induced mitophagy and oxidative stress in mice heart via modulating mitochondrial homeostasis

Di-(2-ethylhexyl) phthalate (DEHP) is a plasticizer that is easily found in the environment. Excessive daily exposure of it may lead to an increased risk of cardiovascular disease (CVD). Lycopene (LYC), as a natural carotenoid, has been shown to have the potential to prevent CVD. However, the mechanism of LYC on cardiotoxicity caused by DEHP exposure is unknown. The research was aimed to investigate the chemoprotection of LYC on the cardiotoxicity caused by DEHP exposure. Mice were treated with DEHP (500 mg/kg or 1,000 mg/kg) and/or LYC (5 mg/kg) for 28 d by intragastric administration, and the heart was subjected to histopathology and biochemistry analysis. The results indicated that DEHP caused cardiac histological alterations and enhanced the activity of cardiac injury indicators, and interfered with mitochondrial function and activating mitophagy. Notably, LYC supplementation could inhibit DEHP-induced oxidative stress. The mitochondrial dysfunction and emotional disorder caused by DEHP exposure were significantly improved through the protective effect of LYC. We concluded that LYC enhances mitochondrial function by regulating mitochondrial biogenesis and dynamics to antagonize DEHP-induced cardiac mitophagy and oxidative stress.

Protective effects of lycopene on TiO2 nanoparticle-induced damage in the liver of mice.

Titanium dioxide nanoparticles (nano-TiO2 ) is one of the most widely used and produced nanomaterials. Studies have demonstrated that nano-TiO2 could induce hepatotoxicity through oxidative stress, and lycopene has strong antioxidant capacity. The present study aimed to explore if lycopene protects the liver of mice from nano-TiO2 damage. Ninety-six ICR mice were randomly divided into eight groups. They were control group, nano-TiO2 -treated group (50 mg/kg BW), lycopene-treated groups (5, 20, and 40 mg/kg BW), and 50 mg/kg BW nano-TiO2 - and lycopene-co-treated groups (nano-TiO2 + 5 mg/kg BW of lycopene, nano-TiO2 + 20 mg/kg BW of lycopene, nano-TiO2 + 40 mg/kg BW of lycopene). After treated by gavage for 30 days, the histopathology of the liver was observed. Liver function was evaluated using changes in serum biochemical indicators of the liver (AST, ALT, ALP); and the level of ROS was indirectly reflected by the level of SOD, GSH-Px, MDA, GSH, and T-AOC. TUNEL assay was performed to examine the apoptosis of hepatocytes. Proteins of p53, cleaved-caspase 9, cleaved-caspase 3, Bcl-2, and Bax as well as p38 were detected. Results showed that lycopene alleviated the liver pathological damage and reduced the injury to liver function induced by nano-TiO2 , as well as decreased nano-TiO2 -induced ROS. Meanwhile, lycopene mitigated apoptosis resulting from nano-TiO2 , accompanied by the reversed expression of apoptosis-related proteins. Furthermore, lycopene significantly reversed the upregulation of p-p38 induced by nano-TiO2 . In conclusion, this study demonstrated that nano-TiO2 resulted in hepatocyte apoptosis through ROS/ROS-p38 MAPK pathway and led to liver function injury. Lycopene protected mice liver against the hepatotoxicity of nano-TiO2 through antioxidant property.

The effect of lycopene on contrast-induced nephrotoxicity in diabetic patients undergoing coronary angiography

Introduction: Radiocontrast nephrotoxicity refers to one of the most prevalent and key complications in diabetic patients. Objectives: This study was aimed to investigate the therapeutic and protective effect of lycopene on contrast-induced nephrotoxicity (CIN) in diabetic patients undergoing coronary angiography. Patients and Methods: In this study, 113 patients who took lycopene with prevention of contrast induced kidney injury regime (lycopene group) or prevention of kidney injury regimen alone (regimen group) were investigated through medical records. Oral lycopene was administered 24 hours before to 72 hours after the angiography. Blood urea nitrogen (BUN), creatinine (Cr), and glomerular filtration rate (GFR) were assessed and recorded in a checklist. SPSS software was conducted for data analysis. Results: At the baseline, there was no significant difference between the mean of urea, Cr, and GFR (P>0.05). However, after administration of lycopene, a significant difference between the mean BUN was observed among groups (P<0.001), with lower rate in the patients taking oral lycopene. Although the mean Cr decreased after the administration of oral lycopene, no statistically significant difference was seen (P = 0.08). The mean GFR was not significant different between the two groups of regimen and lycopene (P=0.44). Conclusion: In patients with diabetes, taking lycopene for CIN may help improve some biochemical factors; nevertheless, its positive effect on the improvement of nephrotoxicity indices cannot be certainly determined.

Lycopene protects against Bisphenol A induced toxicity on the submandibular salivary glands via the upregulation of PPAR-γ and modulation of Wnt/β-catenin signaling

Background and aimThe submandibular salivary glands (SMG) represent a suitable model for studying epithelial cell growth and differentiation. Bisphenol A (BPA) is a xenoestrogen, synthesized to produce polymers such as polycarbonates and epoxy resins. There are concerns about the occurrence of BPA in food, water as well as its appearance in human tissues and body fluids. Lycopene (LYC) is a carotenoid compound that exerts antioxidant and anti-inflammatory properties. This work was performed to study possible protective effect of LYC against BPA toxicity in SMG. Material and Methods40 albino rats were divided into 4 groups; Group I: served as controls. Group II: rats received LYC (4 mg/kg, p.o), Group III: rats received BPA (10 mg/kg, p.o) and Group IV: rats received LYC (4 mg/kg, p.o) and BPA (10 mg/kg, p.o). All drugs were administered for 45 days then under anesthesia, rats were sacrificed. The SMG specimens were taken for histological and biochemical studies. ResultsBPA resulted in a significant rise of malondialdehyde, tumor necrosis factor-α and interleukine-1β. In contrast, the tissue levels of glutathione and PPAR-γ were significantly decreased. BPA activated Wnt/β-catenin pathway evidenced by upregulating WNT3a, β-catenin and c-myc expression. Moreover, SMG of BPA showed degenerative changes that affected the parenchymal and stromal elements of the glands. The immunohistochemical localization of cytokeratin 5,6 and 18 of BPA rats revealed weak immunostaining of the serous secretory cells, myoepithelial cells and ductal cells. Upon treatment with LYC, glutathione and PPAR-γ were restored. ConclusionLYC acted as a protective agent against BPA-induced pathological changes in SMG.

Ratlarda Nikel Sülfatın Genotoksisitesine Karşı Likopenin Koruyucu Etkisi

Aim: Nickel, which has a wide usage area in industries, has teratogenic, carcinogenic, immunotoxic, and genotoxic effects. In this study, the protective effects of lycopene, which has antioxidant properties, were investigated against genotoxicity caused by nickel sulfate. Materials and Methods: In the study, a total of 24 rats (Wistar albino) were divided into four groups: Group I (control) daily by saline intraperitoneal (i.p.) and corn oil oral gavage (0.5 ml); Group II nickel sulfate (20 mg/kg, i.p.) was dissolved in physiological saline; Group III lycopene corn oil (0.5 ml) was suspended by oral gavage at 20 mg/kg doses; Group IV lycopene was suspended in corn oil (0.5 ml) and given by oral gavage at 20 mg/kg doses, 2 hours later, nickel sulfate (20 mg/kg, i.p.) was administered for 21 days. Micronucleated polychromatic erythrocytes (MNPCE) and polychromatic erythrocytes (PCE) were examined by bone marrow micronucleus test, which is one of the genotoxicity tests. Results: It was determined that the administration of lycopene for preventive purposes decreased the MNPCE levels significantly (p

Study on the protective effect of Lycopene on ischemia-reperfusion myocardium through Inhibiting the opening of mitochondrial MPTP and the activation of apoptotic pathway

Through in vitro experiments, the paper investigated whether Lycopene can mitigate cardiac ischemia/reperfusion injury, and further explored whether the underlying mechanism works by inhibiting the opening of MPTP.A hypoxia-reoxygenation model was established. CCK8 was employed to determine the viability of H9c2 cardiomyocytes. LDH was used to determine the degree of damage of H9c2 cardiomyocytes. Trypan blue staining was applied to determine the survival rate of H9c2 cardiomyocytes. Flow cytometry was used to determine the apoptosis rate of H9c2 cardiomyocytes. Rhodamine 123 staining method was applied to evaluate the changes of mitochondrial membrane potential of H9c2 cardiomyocytes. Western blot was employed to determine the protein expressions of related factors of MPTP downstream apoptosis pathway in H9c2 cardiomyocytes. Calcium induction method was used to evaluate the opening degree of MPTP of H9c2 cardiomyocytes. Western blot was applied to determine the protein expressions of the related factors regulating MPTP opening in H9c2 cardiomyocytes.The vitality of H9c2 cardiomyocytes in the Lycopene group was significantly improved, the LDH activity was significantly reduced, and the cell survival rate was significantly improved. The apoptosis rate was significantly reduced, and the membrane potential decreased significantly. The expression levels of Bax, cytochrome C, APAF-1, caspase 9 and caspase-3 proteins were significantly reduced. The sensitivity of MPTP opening was significantly decreased. Lycopene can effectively alleviate the hypoxia/reoxygenation injury of H9c2 cardiomyocytes. By up-regulating Bcl-2 and down-regulating Bax, Lycopene can inhibit the opening of mitochondrial MPTP and the activation of downstream apoptotic pathways, thereby reducing apoptosis.

Protective effects of lycopene on mitochondrial oxidative injury and dysfunction in the liver of aflatoxin B1-exposed broilers

This study was conducted to investigate the effects of lycopene (LYC) on mitochondrial oxidative injury and dysfunction in the liver of aflatoxin B1 (AFB1)-exposed broilers. A total of 192 healthy 1-day-old male broilers were randomly divided into 3 groups with 8 replicates of 8 birds each. Birds in the 3 groups were fed basal diet (control), basal diet with 100 µg/kg AFB1, and basal diet with 100 µg/kg AFB1 and 200 mg/kg LYC, respectively. The experiment lasted 42 d. The results showed that AFB1 decreased average daily body weight gain (ADG), average daily feed intake, and gain to feed ratio (G :F) compared to the control group, the LYC supplementation increased ADG and G/F compared to AFB1 group (P < 0.05). Broilers in the AFB1 group had lower mitochondrial glutathione (mGSH) concentration and glutathione peroxidase (GSH-Px), manganese superoxide dismutase (MnSOD), and thioredoxin reductase activities, and higher hydrogen peroxide (H2O2) and reactive oxygen species (ROS) concentrations than the control group (P < 0.05). The LYC increased mGSH concentration and GSH-Px and MnSOD activities, and decreased H2O2 and ROS concentrations compared to AFB1 group (P < 0.05). Broilers fed the AFB1 diet showed increased mitochondrial swelling and decreased adenosine triphosphate concentration than the control group, and LYC had opposite effects (P < 0.05). The AFB1 decreased the activities of mitochondrial electron transfer chain (ETC) complexes I, II, III, and V, downregulated the mRNA expression levels of hepatic MnSOD, thioredoxin 2, thioredoxin reductase, peroxiredoxin-3, peroxisome proliferator-activated receptor γ coactivator 1α, nuclear respiratory factor 1, and mitochondrial transcription factor A compared with the control group (P < 0.05), and LYC increased activities of mitochondrial ETC complexes III and V, and upregulated mRNA expression levels of these genes in comparison to AFB1 group (P < 0.05). In conclusion, the LYC protected broilers from AFB1-induced liver mitochondrial oxidative injury and dysfunction by stimulating mitochondrial antioxidant capacity and maintaining mitochondrial biogenesis.

Protective effects of lycopene against adenine-induced chronic renal failure in rats

Objectives: Chronic renal failure (CRF) is a public health concern in both developed and developing countries. Therefore, there is still a need to look for secure and successful agents that can either minimise or prevent CRF from advancing to end-stage renal disorder. This study aimed to assess the effect of lycopene on adenine-induced CRF in the rat. Materials and Methods: Animals were divided into five groups (n = 6). Normal control group received normal vehicle, disease control group received orally adenine (50 mg/kg/day), L 100 group received orally lycopene (100 mg/kg/day) + adenine (50 mg/kg/day), L 200 group received orally lycopene (200 mg/kg/day) + adenine (50 mg/kg/day) and L 400 group received orally lycopene (400 mg/kg/day) + adenine (50 mg/kg/day) for 30 days. Results: Compared to the control group, the disease control group had decreased bodyweight, food intake and also increased the relative kidney weight and urine output. Adenine-treated group also significantly increased the blood urea nitrogen, serum creatinine, phosphorus, alkaline phosphatase, uric acid, magnesium and reduced the calcium, urine creatinine and urine urea nitrogen. Besides, adenine also gave a positive test of serum C-reactive protein and proteinuria. Histopathologically, adenine caused significant inflammatory changes to renal tissues compared with the normal control group. When administered concomitantly with adenine, lycopene alleviated all the measured adenine-induced physiological, biochemical and histological changes. Conclusion: We concluded from this analysis that oral lycopene administration could potentially mitigate the adverse effect of CRF that might be due to their antioxidant and free radical scavenging properties.

Lycopene prevents oxygen-glucose deprivation-induced autophagic death in SH-SY5Y cells via inhibition of the oxidative stress-activated AMPK/mTOR pathway.

Lycopene has been reported to exert a protective effect on the brain against transient ischemia‑induced damage; however, whether it could regulate autophagic neuronal death remains elusive. The present study aimed to investigate the role of autophagy in the protective effects of lycopene against neuronal damage and its underlying mechanism. Oxygen‑glucose deprivation (OGD) was used to simulate neuronal ischemic injury in human SH‑SY5Y cells. Lactate dehydrogenase (LDH) release assay revealed that OGD induced SH‑SY5Y cell death. Western blotting demonstrated that OGD upregulated the expression levels of the autophagy marker proteins autophagy protein5(ATG5) and LC3II, but downregulated the autophagy substrate p62 in a time‑dependent manner. By contrast, OGD‑induced cell death was significantly inhibited by the autophagy inhibitors 3‑methyladenine or bafilomycin A1 or by knockdown of ATG5, indicating that OGD may induce autophagic death in SH‑SY5Y cells. Notably, lycopene was shown not only to prevent OGD‑induced SH‑SY5Y cell death, but was also able to effectively inhibit OGD‑induced upregulation of ATG5 and LC3II, and downregulation of p62 in a dose‑dependent manner. Mechanistically, it was suggested that lycopene inhibited OGD‑induced activation of the AMPK/mTOR pathway via attenuation of oxidative stress by maintaining the intracellular antioxidant glutathione (GSH). Furthermore, the inhibitory role of lycopene in GSH depletion was found to be associated with the prevention of OGD‑induced depletion of intracellular cysteine and downregulation of xCT. Collectively, the present study demonstrated that lycopene protected SH‑SY5Y cells against OGD‑induced autophagic death by inhibiting oxidative stress‑dependent activation of the AMPK/mTOR pathway.

Lycopene mitigates arsenic-induced nephrotoxicity with activation of the Nrf2 pathway in mice

This study was designed to investigate the potential protective effect of lycopene (Lyc) against arsenic-induced nephrotoxicity. Sodium arsenite orally administered to mice for 14 days, inducing severe nephrotoxicity, in the form of hyponatremia, hyperkalemia, and elevation in the markers of kidney damage. Induction of severe inflammation, apoptosis, and oxidants/antioxidants imbalance was observed in kidney tissues. DNA damage in the form of 8-hydroxy-2′deoxyguanosine was found. However, pretreatment with Lyc prevented these consequences of arsenic poisoning in the kidneys. We suggest that Lyc exerts its nephroprotective effect via the Nrf2/HO-1 pathway, making it a promising prophylactic agent against arsenic toxicity.

The protective effect of lycopene against oxidative kidney damage associated with combined use of isoniazid and rifampicin in rats.

It is known that the combined use of antibiotics, such as isoniazid and rifampicin, in the treatment of tuberculosis causes oxidative kidney damage. The aim of this study was to biochemically and histopathologically investigate the effect of lycopene on oxidative kidney damage due to the administration of isoniazid and rifampicin in albino Wistar male rats. Lycopene at a dose of 5 mg/kg was orally administered to lycopene+isoniazid+rifampicin (LIR) rats, and normal sunflower oil (0.5 mL) was orally administered to isoniazid+rifampicin (IR) and healthy control (HG) rats as vehicle by gavage. One hour after the administration of lycopene and vehicle, 50 mg/kg isoniazid and rifampicin were given orally to the LIR and IR groups. This procedure was performed once a day for 28 days. Rats were sacrificed by a high dose of anesthesia at the end of this period, and oxidant-antioxidant parameters were measured in the removed kidney tissues. Creatinine and blood urea nitrogen (BUN) levels were measured in blood samples, and kidney tissues were also evaluated histopathologically. The combined administration of isoniazid and rifampicin changed the oxidant-antioxidant balance in favor of oxidants, and it increased blood urea nitrogen and creatinine levels, which are indicators of kidney function. Co-administration of isoniazid and rifampicin also caused oxidative kidney damage. Lycopene biochemically and histopathologically decreased oxidative kidney damage induced by isoniazid and rifampicin administration. These results suggested that lycopene may be beneficial in the treatment of nephrotoxicity due to isoniazid and rifampicin administration.

Effect of lycopene on hepatotoxicity induced by perfluorooctane sulfonic acid in rats

Objective: Intend to observe the liver injury induced by perfluorooctane sulfonic acid (PFOS) in SD rats and the protective effect of lycopene (LP) and its possible mechanism. Methods: 48 SD rats were randomly divided into 8 groups. The solvent control group of LP protection group and LP protection low, middle and high dose PFOS exposure groups were given LP suspension once a day according to their designed dose. The contents of ALT, ASP and AST in serum, the content of MDA in liver tissue and the activity of SOD and GSH-Px in liver tissue were measured after 2 months. Results: The levels of serum ALT, AST and serum ASP enzyme activity in middle and high dose PFOS groups and high dose PFOS groups were significantly higher than those in solvent control group (P < 0 05).The levels of serum ALT, ALP and AST in middle and high dose PFOS groups protected by LP were lower than those in the same dose PFOS group (P < 0 05). The content of MDA in liver tissue of rats treated with LP was significantly lower than that of rats exposed to the same dose of PFOS (P < 0.05). The contents of GSH-Px and SOD in the liver homogenate of the low, middle and high dose PFOS groups decreased compared with the solvent control group. Conclusion: PFOS can induce liver injury in rats, and lycopene can antagonize liver injury induced by PFOS through antioxidant mechanism.

The Protective Effect of Lycopene on Prostate Growth Inhibitory Efficacy by Decreasing Insulin Growth Factor-1 in Indonesian Human Prostate Cancer Cells.

IntroductionLycopene has been discussed as a potential effector in the prevention and therapy of prostate cancer. It is red, lipophilic and naturally occurring in many fruits and vegetables, such as tomatoes. Several growth factors, including insulin-like growth factor 1 (IGF-1), play important roles in carcinogenesis and metastasis. IGF-1 is a mitogen that plays important roles in the regulation of proliferation, differentiation, and apoptosis. Binding of IGF-1 to its cognate membrane receptor activates Ras/Raf/MAP kinase signaling pathways, which regulate cell-cycle progression, cell survival, and transformation. Lycopene has its protective effect, which affects multiple IGF-1-activated signaling pathways. Lycopene stimulates apoptosis through intrinsic pathways, by stimulating the pro-apoptotic factor of the mitochondrial cavity such as the Bax/Bak protein (an apoptotic promotor). Although tomatoes are widely consumed in Indonesia, there is no research study about the effect of lycopene on prostate cancer in Indonesia. Hence, this study is conducted to measure the influence of lycopene on the level of IGF-1 in Indonesian human prostate cancer cells.Materials and MethodsProstate cancer cells were studied. In this experimental study, cells were taken from patients with Gleason score 6 and divided into 5 groups: 2 control groups and 3 treatment groups, which were given 1 µM, 2 µM and 4 µM of lycopene, respectively. Measurement of mean IGF-1 level was performed by ELISA. A comparative analysis was performed by two-way ANOVA.ResultsThe result showed that there was a significant difference in mean IGF-1 levels in the provision of various concentrations of lycopene and time of observation (p<0.05). Increased level of mean IGF-1 appeared on 2µM dose of lycopene at 48 hours observation and began to decline in 72 hours observation. This happened also on 4µM lycopene at 24 hours observation and began to decline in 48 hours observation (p<0.05).ConclusionLycopene could be administered as adjuvant therapy for prostate cancer patients to increase apoptosis, and eventually inhibit the progressivity of cancer cells.

Protective effects of lycopene on hippocampal neurotoxicity and memory impairment induced by bisphenol A in rats.

Bisphenol A (BPA) is used to produce polycarbonate plastic and epoxy resins which are used in many consumer products. Most people encounter BPA in their daily routines. However, it has been heavily reported that BPA has a neurotoxic effect. The present study aimed to investigate the effect of lycopene on cognitive deficits induced by a high dose of BPA focusing on mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway, oxidative stress, apoptosis, and memory retrieval in adult male rats. Therefore, 72 rats were divided into four groups: control group, BPA group (50 mg/kg body weight (bw)) 3 days a week for 42 days, lycopene group (10 mg/kg bw) daily for 42 days, and lycopene + BPA group. Concurrent treatment of lycopene with BPA improved the learning and cognition memory in Morris water maze and novel object recognition tests along with an increase in acetylcholine esterase activity as well as inhibition of oxidative stress by restoring reduced glutathione and suppressing malondialdehyde hippocampal level to their normal levels. Mechanistically, lycopene upregulated the protein expression of tyrosine receptor kinase B, which resulted in an upsurge in its downstream cascades MAPK/ERK1/2/cAMP response element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathway in the hippocampus of BPA-intoxicated rats. Furthermore, concurrent treatment of lycopene with BPA prevented apoptosis by marked decrease in Bcl-2 associated X protein (Bax) gene expression and caspase 3 activity while restoring B-cell leukemia/lymphoma-2 (Bcl-2) gene expression. In conclusion, the present study provided evidence that lycopene exerted a neuroprotective effect against BPA intoxication in hippocampi of rats via its antioxidant properties, activation of MAPK/ERK pathway, and inhibiting a neuronal apoptosis which reflected on improving the learning and cognition memory.

Protective Effect of Lycopene against Reperfusion Injury in Rats with Ovarian Torsion: A Biochemical and Histopathological Evaluation.

Objective The aim of our study was to evaluate the effect of two different doses of lycopene, an antioxidant, on experimentally induced ovarian ischemia/reperfusion (IR) injury in rat model. Materials and Methods Twenty-four female rats were randomly divided into four groups: sham operation (group 1), 3-hour ischemia, 3-hour reperfusion (IR) (group 2), and IR + 100 mg/kg lycopene (PO) (group 3), IR + 200 mg/kg of lycopene (group 4). The rats’ superoxide dismutase (SOD), myeloperoxidase (MPO) activities, malondialdehyde (MDA), and glutathione (GSH) levels were calculated. Ovarian tissue damage was assessed using a histopathological scoring system. Results Serum parameter levels and histological scores showed that treatment with lycopene may be conservative approach to prevent IR injury after the ovarian detorsion procedure.The improvement with lycopene was higher at 200 mg than at 100 mg. The MPO and MDA values were significantly lower in groups 3 and 4 as compared with group 2 ( p < 0.05), whereas the MPO and MDA values were lower in group 4 as compared with group 3.The SOD and GSH values were significantly higher in groups 3 and 4 as compared with group 2 ( p < 0.05), whereas the SOD and GSH values were higher in group 4 as compared with group 3.Tissue damage scores were elevated in the IR group compared with the sham group, but the treatment with different lycopene doses after reperfusion improved the histopathological tissue damage scores. Conclusion The results showed that lycopene treatment reduced ovarian IR damage. Antioxidant activity was found to increase in a dose-dependent manner. Lycopene treatment may be conservative approach for ovarian torsion patients after the detorsion procedure to prevent IR damage.

Protective effects of lycopene against AFB1-induced erythrocyte dysfunction and oxidative stress in mice

To evaluate the protective role of lycopene (LYC) against aflatoxin B1 (AFB1)-induced erythrocyte dysfunction and oxidative stress, male kunming mice were treated with LYC (5 mg/kg) and/or AFB1 (0.75 mg/kg) by intragastric administration for 30 d. Hematological indices were detected to assess erythrocyte function. The erythrocytes C3b receptor rate (E-C3bRR) and erythrocytes C3b immune complex rosette rate (E-ICRR) were detected to assess erythrocyte immune function. Hydrogen peroxide (H2O2) and malondialdehyde (MDA) contents and superoxide dismutase (SOD) and catalase (CAT) activities were determined to evaluate erythrocyte oxidative stress. The results showed that LYC administration significantly relieved AFB1-induced erythrocyte dysfunction by increasing the levels of red blood cell count (RBC), hemoglobin (HGB) and hematocrit (HCT), as well as reducing red blood cell volume distribution width (RDW) level, while the levels of mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC) and mean platelet volume (MPV) had no significant differences among the four groups. Besides, LYC ameliorated AFB1-induced erythrocyte immune dysfunction by increasing E-C3bRR and decreasing E-ICRR. Furthermore, LYC also alleviated AFB1-induced erythrocyte oxidative stress by decreasing H2O2 and MDA contents and increasing SOD and CAT activities. These results indicated that LYC protected against AFB1-induced erythrocyte dysfunction and oxidative stress in mice. The findings could lead a possible therapeutics for the management of AFB1-induced erythrocyte toxicity.