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Head of Institute: Prof. Oren Froy

Administrative manager: Ms. Yael Fruchter

Office Address:
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Robert H. Smith Faculty of Agriculture, Food and Environment,
The Hebrew University of Jerusalem, 
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Publications

2019
Miron, N. ; Tirosh, O. Cholesterol Prevents Hypoxia-Induced Hypoglycemia by Regulation of a Metabolic Ketogenic Shift. Oxidative Medicine and Cellular Longevity 2019, 2019. Publisher's VersionAbstract
Blood cholesterol levels have been connected to high-altitude adaptation. In the present study, we treated mice with high-cholesterol diets following exposure to acute hypoxic stress and evaluated the effects of the diets on whole-body, liver glucose, and liver fat metabolism. For rapid cholesterol liver uptake, 6-week-old male C57BL/J6 mice were fed with high-cholesterol/cholic acid (CH) diet for 6 weeks and then were exposed to gradual oxygen level reduction for 1 h and hypoxia at 7% oxygen for additional 1 hour using a hypoxic chamber. Animals were than sacrificed, and metabolic markers were evaluated. Hypoxic treatment had a strong hypoglycemic effect that was completely blunted by CH treatment. Decreases in gluconeogenesis and glycogenolysis as well as an increase in ketone body formation were observed. Such changes indicate a metabolic shift from glucose to fat utilization due to activation of the inducible nitric oxide synthase/AMPK axis in the CH-treated animals. Increased ketogenesis was also observed in vitro in hepatocytes after cholesterol treatment. In conclusion, our results show for the first time that cholesterol contributes to metabolic shift and adaptation to hypoxia in vivo and in vitro through induction of HIF-1α and iNOS expression. © 2019 Naama Miron and Oren Tirosh.
Anavi, S. ; Tirosh, O. iNOS as a metabolic enzyme under stress conditions. Free Radical Biology and Medicine 2019. Publisher's VersionAbstract
Nitric oxide (NO) is a free radical acting as a cellular signaling molecule in many different biochemical processes. NO is synthesized from L-arginine through the action of the nitric oxide synthase (NOS) family of enzymes, which includes three isoforms: endothelial NOS (eNOS), neuronal NOS (nNOS) and inducible NOS (iNOS). iNOS-derived NO has been associated with the pathogenesis and progression of several diseases, including liver diseases, insulin resistance, obesity and diseases of the cardiovascular system. However, transient NO production can modulate metabolism to survive and cope with stress conditions. Accumulating evidence strongly imply that iNOS-derived NO plays a central role in the regulation of several biochemical pathways and energy metabolism including glucose and lipid metabolism during inflammatory conditions. This review summarizes current evidence for the regulation of glucose and lipid metabolism by iNOS during inflammation, and argues for the role of iNOS as a metabolic enzyme in immune and non-immune cells. © 2019
Kanner, J. ; Shpaizer, A. ; Nelgas, L. ; Tirosh, O. S-Nitroso- N-acetylcysteine (NAC-SNO) as an Antioxidant in Cured Meat and Stomach Medium. Journal of Agricultural and Food Chemistry 2019, 67, 10930-10936. Publisher's VersionAbstract
The stability of lipids in meat products depends on the initial concentration of hydroperoxides, the catalytic involvement of metal ions and myoglobin, endogenous antioxidants, and biological and technological factors. Ground meat was treated with additives, sealed in vacuum bags, heated to 75 °C, and stored opened to air at 4 °C. S-Nitroso-N-acetylcysteine (NAC-SNO) at concentration like nitrite used by the industry prevents lipid peroxidation in the product, even after storage for 1 month at 4 °C. The same simulated treatments at different concentrations of both compounds show that NAC-SNO acts as an antioxidant ∼4-fold better than nitrite at pH 6.2 or 3.0. Ascorbic acid significantly improves nitrite antioxidant effect. NAC-SNO was found to prevent, much better than nitrite, accumulation of reactive aldehydes and hydroxynonenal protein modification. In condition like those used by the industry for meat products processing, NAC-SNO acts better than nitrite to provide antioxidant protection without the side effect of N-nitrosation, oxidation, and the loss of nutrient generated by nitrite. © 2019 American Chemical Society.
Abu Ahmad, N. ; Raizman, M. ; Weizmann, N. ; Wasek, B. ; Arning, E. ; Bottiglieri, T. ; Tirosh, O. ; Troen, A. M. Betaine attenuates pathology by stimulating lipid oxidation in liver and regulating phospholipid metabolism in brain of methionine-choline–deficient rats. The FASEB Journal 2019, fj.201802683R. Publisher's VersionAbstract
Methyl-donor deficiency is a risk factor for neurodegenerative diseases. Dietary deficiency of the methyl-donors methionine and choline [methionine-choline?deficient (MCD) diet] is a well-established model of nonalcoholic steatohepatitis (NASH), yet brain metabolism has not been studied in this model. We hypothesized that supplemental betaine would protect both the liver and brain in this model and that any benefit to the brain would be due to improved liver metabolism because betaine is a methyl-donor in liver methylation but is not metabolically active in the brain. We fed male Sprague-Dawley rats a control diet, MCD diet, or betaine-supplemented MCD (MCD+B) diet for 8 wk and collected blood and tissue. As expected, betaine prevented MCD diet?induced NASH. However, contrary to our prediction, it did not appear to do so by stimulating methylation; the MCD+B diet worsened hyperhomocysteinemia and depressed liver methylation potential 8-fold compared with the MCD diet. Instead, it significantly increased the expression of genes involved in ?-oxidation: fibroblast growth factor 21 and peroxisome proliferator?activated receptor α. In contrast to that of the liver, brain methylation potential was unaffected by diet. Nevertheless, several phospholipid (PL) subclasses involved in stabilizing brain membranes were decreased by the MCD diet, and these improved modestly with betaine. The protective effect of betaine is likely due to the stimulation of ?-oxidation in liver and the effects on PL metabolism in brain.?Abu Ahmad, N., Raizman, M., Weizmann, N., Wasek, B., Arning, E., Bottiglieri, T., Tirosh, O., Troen, A. M. Betaine attenuates pathology by stimulating lipid oxidation in liver and regulating phospholipid metabolism in brain of methionine-choline?deficient rats.Methyl-donor deficiency is a risk factor for neurodegenerative diseases. Dietary deficiency of the methyl-donors methionine and choline [methionine-choline?deficient (MCD) diet] is a well-established model of nonalcoholic steatohepatitis (NASH), yet brain metabolism has not been studied in this model. We hypothesized that supplemental betaine would protect both the liver and brain in this model and that any benefit to the brain would be due to improved liver metabolism because betaine is a methyl-donor in liver methylation but is not metabolically active in the brain. We fed male Sprague-Dawley rats a control diet, MCD diet, or betaine-supplemented MCD (MCD+B) diet for 8 wk and collected blood and tissue. As expected, betaine prevented MCD diet?induced NASH. However, contrary to our prediction, it did not appear to do so by stimulating methylation; the MCD+B diet worsened hyperhomocysteinemia and depressed liver methylation potential 8-fold compared with the MCD diet. Instead, it significantly increased the expression of genes involved in ?-oxidation: fibroblast growth factor 21 and peroxisome proliferator?activated receptor α. In contrast to that of the liver, brain methylation potential was unaffected by diet. Nevertheless, several phospholipid (PL) subclasses involved in stabilizing brain membranes were decreased by the MCD diet, and these improved modestly with betaine. The protective effect of betaine is likely due to the stimulation of ?-oxidation in liver and the effects on PL metabolism in brain.?Abu Ahmad, N., Raizman, M., Weizmann, N., Wasek, B., Arning, E., Bottiglieri, T., Tirosh, O., Troen, A. M. Betaine attenuates pathology by stimulating lipid oxidation in liver and regulating phospholipid metabolism in brain of methionine-choline?deficient rats.
2018
Shpaizer, A. ; Nussinovitch, A. ; Kanner, J. ; Tirosh, O. S-Nitroso-N-acetylcysteine Generates Less Carcinogenic N-Nitrosamines in Meat Products than Nitrite. J Agric Food Chem 2018, 66, 11459-11467.Abstract
Nitrite reacts with secondary amines to form N-nitrosamines (N-NA), which lead to gastrointestinal cancers. The aim of this study was to compare nitrite with S-nitrosocysteine (Cys-SNO) and S-nitroso-N-acetylcysteine (NAC-SNO) with respect to N-NA formation, which was evaluated by determining the conversion of N-methylaniline to N-nitrosomethylaniline. Under neutral and acidic pH conditions, N-NA formation rate was nitrite > Cys-SNO > NAC-SNO. In the presence of copper or nucleophiles, NAC-SNO generated much less N-NA than Cys-SNO. Nitrite and Cys-SNO produced higher amounts of N-NA in the presence of oxygen, whereas NAC-SNO was almost oxygen insensitive. In meat in the stomach medium, NAC-SNO produced much lower amounts of N-NA than other additives. In heated meat, Cys-SNO and NAC-SNO generated the nitrosyl-hemochrome pink pigment, better than nitrite. In conclusion, NAC-SNO was much less reactive for N-NA formation than nitrite and Cys-SNO in conditions relevant to meat production and stomach digestion.
Tirosh, O. Hypoxic Signaling and Cholesterol Lipotoxicity in Fatty Liver Disease Progression. Oxid Med Cell Longev 2018, 2018, 2548154.Abstract
Cholesterol is the only lipid whose absorption in the gastrointestinal tract is limited by gate-keeping transporters and efflux mechanisms, preventing its rapid absorption and accumulation in the liver and blood vessels. In this review, I explored the current data regarding cholesterol accumulation in liver cells and key mechanisms in cholesterol-induced fatty liver disease associated with the activation of deleterious hypoxic and nitric oxide signal transduction pathways. Although nonalcoholic fatty liver disease (NAFLD) affects both obese and nonobese individuals, the mechanism of NAFLD progression in lean individuals with healthy metabolism is puzzling. Lean NAFLD individuals exhibit normal metabolic responses, implying that liver damage is not associated with impaired metabolism per se and that direct lipotoxic effects are crucial for disease progression. Several redox and oxidant signaling pathways involving cholesterol are at play in fatty liver disease development. These include impairment of the mitochondrial and lysosomal function by cholesterol loading of the inner-cell membranes; formation of cholesterol crystals and hepatocyte degradation; and crown-like structures surrounding degrading hepatocytes, activating Kupffer cells, and evoking inflammation. The current review focuses on the induction of liver inflammation, fibrosis, and steatosis by free cholesterol via the hypoxia-inducible factor 1 (HIF-1), a main oxygen-sensing transcription factor involved in all stages of NAFLD. Cholesterol loading in hepatocytes can result in chronic HIF-1 activity because of the decreased oxygen availability and excessive production of nitric oxide and mitochondrial reactive oxygen species.
Shtriker, M. G. ; Peri, I. ; Taieb, E. ; Nyska, A. ; Tirosh, O. ; Madar, Z. Galactomannan More than Pectin Exacerbates Liver Injury in Mice Fed with High-Fat, High-Cholesterol Diet. Molecular Nutrition & Food Research 2018, 62, 1800331. Publisher's VersionAbstract
Scope Galactomannan and citrus pectin are considered ?super fibers? known for altering gut microbiota composition and improving glucose and lipid metabolism. The study aims to investigate the fiber's effect on a nonalcoholic steatohepatitis (NASH) model. Methods and results Two feeding experiments are carried out using groups of 7?8 week-old male C57BL/6J mice. The diets used are based on a high cholesterol/cholate diet (HCD), such as a nutritional NASH model. Mice are fed a diet with or without 15% fiber-citrus pectin (HCD-CP) or galactomannan (HCD-G) together with the HCD (first experiment), which commenced 3 weeks prior to the HCD (second experiment). Liver damage is evaluated by histological and biochemical parameters. Galactomannan leads to lesser weight gain and improved glucose tolerance, but increased liver damage. This is shown by elevated levels of liver enzymes compared to that with HCD alone. Fibers induce higher steatosis, as evaluated by liver histology. This intriguing result is linked to various changes in the gut microbiota, such as elevated Proteobacteria levels in the galactomannan group, which are correlated with disturbed metabolism and dysbiosis. Conclusions In a NASH mouse model, galactomannan increases liver damage but improves glucose metabolism. Changes in the microbiota composition may answer this enigmatic observation.
Shtriker, M. G. ; Hahn, M. ; Taieb, E. ; Nyska, A. ; Moallem, U. ; Tirosh, O. ; Madar, Z. Fenugreek galactomannan and citrus pectin improve several parameters associated with glucose metabolism and modulate gut microbiota in mice. Nutrition 2018, 46, 134 - 142.e3. Publisher's VersionAbstract
ObjectiveGalactomannans derived from fenugreek confer known health benefits; however, there is little information regarding health benefits of citrus pectin (CP) and its association with gut microbiome metabolites. The aim of this study was to examine links between galactomannan and CP consumption, microbiota development, and glucose metabolism. Design Male C57 BL/6 J mice ages 7 to 8 wk were fed ad libitum with a normal diet or one supplemented with 15% of either galactomannan or CP. At 3 wk, an oral glucose tolerance test was performed. Animals were sacrificed at 4 wk and relevant organs were harvested. Results Fiber enrichment led to reductions in weight gain, fasting glucose levels, and total serum cholesterol (P < 0.05). Compared with mice fed the normal diet, microbiota populations were altered in both fiber groups and were found to be richer in Bacteroidetes rather than Firmicutes (P < 0.05). The modification was significantly greater in galactomannan-fed than in CP-fed mice (P < 0.0001). Also, enhanced levels of the short-chain fatty acid (SCFA) propionate were found in the cecal contents of CP-fed animals (P < 0.05). Protein expression levels of monocarboxylate transporter 1, which may promote transport of SCFA, were measured in the large intestines after fiber consumption. Enhanced adenosine monophosphate-activated protein kinase (AMPK) activation was observed in livers of galactomannan-fed mice (P < 0.05). Conclusion Consumption of diets containing soluble fibers, as used in this study, resulted in gut microbiota comprising a healthier flora, and led to positive effects on weight, glycemic control, and liver β oxidation via AMPK.
Meidan, E. ; Kolesnikov, Y. ; Tirosh, O. High Fat Diets Composed of Palm Stearin and Olive Oil Equally Exacerbate Liver Inflammatory Damage and Metabolic Stress in Mice. Molecular Nutrition & Food Research 2018, 62, 1700915. Publisher's VersionAbstract
Scope People with fatty liver could be subject to acute infections such as sepsis. The aim of the study is to evaluate the effect of high fat diets (HFD) of olive oil and palm stearin on liver inflammation induced by lipopolysaccharides (LPS). Methods and results C57BL/6J male mice were treated with high fat diets with different sources of oils: palm stearin and olive oil for 8 weeks followed by LPS injection. The proinflammatory effect of olive oil was also studied using gavage treatment and IP injection of LPS. Animals fed with HFDs showed an increase in body weight, elevated blood glucose levels, and fatty liver phenotype. HFDs aggravated the effect of LPS treatment to induce inflammatory response compared to low fat diet (LFD) effect. Following HFD supplementation, LPS induced hyperinsulinemia, more liver damage than in animals that consumed LFD. In addition, both gavage and long-term feeding with high lipids in the presence of LPS resulted in inhibition of gluconeogenic genes expression. Conclusion HFDs of both monounsaturated and saturated fat potentiated liver inflammation induced by LPS treatment indicate that the total amount of fat consumed is the main proinflammatory factor rather than the type of fat.
2017
Shefer-Weinberg, D. ; Sasson, S. ; Schwartz, B. ; Argov-Argaman, N. ; Tirosh, O. Deleterious effect of n-3 polyunsaturated fatty acids in non-alcoholic steatohepatitis in the fat-1 mouse model. Clinical Nutrition Experimental 2017, 12, 37 - 49. Publisher's VersionAbstract
Summary Non-alcoholic fatty liver disease (NAFLD) represents a spectrum of pathologies, ranging from hepatocellular steatosis to non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis. It has been suggested that fish oil containing n-3 polyunsaturated fatty acids (n-3 PUFA) induce beneficial effects in NAFLD. However, n-3 PUFA are sensitive to peroxidation that generate free radicals and reactive aldehydes. We aimed at determining whether changing the tissue ratio of n-3 to n-6 PUFA may be beneficial or alternatively harmful to the etiology of NAFLD. The transgenic Fat-1 mouse model was used to determine whether n-3 PUFA positively or negatively affect the development of NAFLD. fat-1mice express the fat-1 gene of Caenorhabditis elegans, which encodes an n-3 fatty-acid desaturase that converts n-6 to n-3 fatty acids. Wild-type C57BL/6 mice served as the control group. Both groups of mice were fed methionine and choline deficient (MCD) diet, which induces NASH within 4 weeks. The study shows that NASH developed faster and was more severe in mice from the fat-1 group when compared to control C57BL/6 mice. This was due to enhanced lipid peroxidation of PUFA in the liver of the fat-1 mice as compared to the control group. Results of our mice study suggest that supplementing the diet of individuals who develop or have fatty livers with n-3 PUFA should be carefully considered and if recommended adequate antioxidants should be added to the diet in order to reduce such risk.
Kanner, J. ; Selhub, J. ; Shpaizer, A. ; Rabkin, B. ; Shacham, I. ; Tirosh, O. Redox homeostasis in stomach medium by foods: The Postprandial Oxidative Stress Index (POSI) for balancing nutrition and human health. Redox Biol 2017, 12, 929-936.Abstract
Red-meat lipid peroxidation in the stomach results in postprandial oxidative stress (POS) which is characterized by the generation of a variety of reactive cytotoxic aldehydes including malondialdehyde (MDA). MDA is absorbed in the blood system reacts with cell proteins to form adducts resulting in advanced lipid peroxidation end products (ALEs), producing dysfunctional proteins and cellular responses. The pathological consequences of ALEs tissue damage include inflammation and increased risk for many chronic diseases that are associated with a Western-type diet. In earlier studies we used the simulated gastric fluid (SGF) condition to show that the in vitro generation of MDA from red meat closely resembles that in human blood after consumption the same amount of meat. In vivo and in vitro MDA generations were similarly suppressed by polyphenol-rich beverages (red wine and coffee) consumed with the meal. The present study uses the in vitro SGF to assess the capacity of more than 50 foods of plant origin to suppress red meat peroxidation and formation of MDA. The results were calculated as reducing POS index (rPOSI) which represents the capacity in percent of 100g of the food used to inhibit lipid peroxidation of 200g red-meat a POSI enhancer (ePOSI). The index permitted to extrapolate the need of rPOSI from a food alone or in ensemble such Greek salad, to neutralize an ePOSI in stomach medium, (ePOS-rPOSI=0). The correlation between the rPOSI and polyphenols in the tested foods was R=0.75. The Index was validated by comparison of the predicted rPOSI for a portion of Greek salad or red-wine to real inhibition of POS enhancers. The POS Index permit to better balancing nutrition for human health.
Anavi, S. ; Madar, Z. ; Tirosh, O. Non-alcoholic fatty liver disease, to struggle with the strangle: Oxygen availability in fatty livers. Redox Biol 2017, 13, 386-392.Abstract
Nonalcoholic fatty liver diseases (NAFLD) is one of the most common chronic liver disease in Western countries. Oxygen is a central component of the cellular microenvironment, which participate in the regulation of cell survival, differentiation, functions and energy metabolism. Accordingly, sufficient oxygen supply is an important factor for tissue durability, mainly in highly metabolic tissues, such as the liver. Accumulating evidence from the past few decades provides strong support for the existence of interruptions in oxygen availability in fatty livers. This outcome may be the consequence of both, impaired systemic microcirculation and cellular membrane modifications which occur under steatotic conditions. This review summarizes current knowledge regarding the main factors which can affect oxygen supply in fatty liver.
2016
Rozenboim, I. ; Mahato, J. ; Cohen, N. A. ; Tirosh, O. Low protein and high-energy diet: a possible natural cause of fatty liver hemorrhagic syndrome in caged White Leghorn laying hens. Poultry Scienceps 2016, 95, 612 - 621. Publisher's VersionAbstract
Fatty liver hemorrhagic syndrome (FLHS) is a metabolic condition of chicken and other birds caused by diverse nutritional, hormonal, environmental, and metabolic factors. Here we studied the effect of different diet composition on the induction of FLHS in single comb White Leghorn (WL) Hy-line laying hens. Seventy six (76) young WL (26 wks old) laying hens and 69 old hens (84 wks old) of the same breed were each divided into 4 treatment groups and provided 4 different diet treatments. The diet treatments included: control (C), 17.5% CP, 3.5% fat (F); normal protein, high fat (HF), 17.5% CP, 7% F; low protein, normal fat (LP), 13% CP, 3.5% F; and low protein, high fat (LPHF), 13% CP, 6.5% F. The diets containing high fat also had a higher ME of 3,000 kcal/kg of feed while the other 2 diets with normal fat had a regular lower amount of ME (2750 kcal/kg). Hen-day egg production (HDEP), ADFI, BW, egg weight, plasma enzymes indicating liver damage (alkaline phosphatase [ALP], aspartate aminotransferase [AST], gamma-glutamyl transferase [GGT]), liver and abdominal fat weight, liver color score (LCS), liver hemorrhagic score (LHS), liver fat content (LFC), liver histological examination, lipid peroxidation product in the liver, and genes indicating liver inflammation were evaluated. HDEP, ADFI, BW, and egg weight were significantly decreased in the LPHF diet group, while egg weight was also decreased in the LP diet group. In the young hens (LPHF group), ALP was found significantly higher at 30 d of diet treatment and was numerically higher throughout the experiment, while AST was significantly higher at 105 d of treatment. LCS, LHS, and LFC were significantly higher in young hens on the LPHF diet treatment. A liver histological examination shows more lipid vacuolization in the LPHF treatment diet. HF or LP alone had no significant effect on LFC, LHS, or LCS. We suggest that LP in the diet with higher ME from fat can be a possible natural cause for predisposing laying hens to FLHS.
Hirsch, N. ; Konstantinov, A. ; Anavi, S. ; Anna Aronis, ; Hagay, Z. ; Madar, Z. ; Tirosh, O. Prolonged feeding with green tea polyphenols exacerbates cholesterol-induced fatty liver disease in mice. Molecular Nutrition & Food ResearchMolecular Nutrition & Food ResearchMol. Nutr. Food Res. 2016, 60, 2542 - 2553. Publisher's VersionAbstract
Scope This study investigated the potential deleterious impact of dietary supplementation with green tea extract (GTE) on the progression of fatty liver disease, in a mouse model of cholesterol-induced steatohepatitis that represents chronic liver injury. Methods and results Male C57BL mice (n = 32, 8-wk-old) were fed for 6 wk with one of the following diets: normal control diet (ND, Con), Con + 1% w/w polyphenols from GTE (Con + GTE); high cholesterol diet, Con + 1% cholesterol + 0.5% cholate w/w (HCD); HCD + 1% green tea polyphenols w/w (HCD + GTE). Hepatic steatosis, oxidative, and inflammatory markers and bile acid synthesis pathways were measured. HCD supplementation resulted in hepatic steatosis and liver damage. In animals supplemented with the HCD + GTE an exacerbated hepatic steatosis, oxidative stress, and inflammatory response were observed compared to HCD supplemented animals. HCD + GTE supplementation elevated blood levels of liver enzymes and serum bile acids compared HCD-treated animals. HCD + GTE supplementation altered bile acid synthesis in the cholesterol clearance pathway, inducing a shift from the classically regulated CYP7A1 pathway to the alternative acidic pathway. Conclusion Prolonged GTE supplementation dramatically increased hepatic oxidative stress, inflammation and liver injury, and altered the bile acid synthesis pathway in mice fed a HCD.
Tal, Y. ; Anavi, S. ; Reisman, M. ; Samach, A. ; Tirosh, O. ; Troen, A. M. The neuroprotective properties of a novel variety of passion fruit. Journal of Functional Foods 2016, 23, 359 - 369. Publisher's VersionAbstract
Passion fruit is a commercially important crop. The neuroprotective activity of fruit extracts from two hybrid lines of antioxidant ester thiol-rich Passiflora edulis Sims, the commercial “Passion Dream” and novel cultivar 428 (“Dena”) line were studied. Crude extracts from line 428 displayed the strongest dose-dependent neuroprotective activity, preventing glutamate induced cell-death, mitochondrial depolarization and glutathione depletion, when added to the medium of cultured HT4 neurons (p < 0.05). Supplementing diet of mice with the 428 fruit-extract improved survival of dopaminergic neurons by 60% in mice injected with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MTPT) compared to control-fed MPTP-injected mice (p < 0.05). The neuroprotection conferred by passion fruit extracts in vivo and in vitro shows promise for further research into their bioactive potential for medical exploitation.