Abstract

Tomato is a horticultural crop of interest, that is widely consumed fresh or as processed products. The present investigation was to evaluate the antioxidant indices (total phenolic content, flavonoid content, ferric reducing antioxidant power, radical scavenging activities, inhibitory action against lipid oxidation) and anti-cholinesterase action (acetylcholinesterase and butyrylcholinesterase) of tomato fruits (ripe and unripe) and pastes (paste 2 and paste 1) after simulated gastrointestinal digestion. The total phenolic content (mg/g GAE) of the In vitro digested tomato fruits and pastes showed higher values (ripe tomato: 61.08; tomato paste1: 56.02; tomato paste 2: 60.36; unripe tomato: 38.97) than the ethanolic extracts, with digested ripe tomato ranking higher. Similar results were also obtained for total flavonoid content, ferric reducing antioxidant power, and the radical scavenging activities (DPPH*, ABTS˙+, NO*, OH*), with the in vitro digested samples ranking high. The ability of the enzyme digested and ethanolic extracts of tomato fruits and pastes to inhibit iron and sodium nitroprusside induced lipid oxidation in rat’s liver and brain homogenate increased in a concentration dependent manner, with the enzyme digested tomato fruits and pastes ranking high. Similarly, the ability of the in vitro digested tomato fruit and pastes to enhance activities of the antioxidant enzymes (GPx, GSH, SOD and Catalase) and to inhibit the formation of cholinesterases ranked high. The result of this investigation showed that the studied tomato fruit and pastes possess antioxidant and anti-cholinesterase activities that would be bio-available after the gastrointestinal digestion and by implication could be harnessed as functional food.

Highlights

  • The result of the total phenolic content (TPC), is as presented on Table 1.The results revealed a higher TPC for all in vitro enzyme-digested tomato samples than the ethanolic extracts

  • The result further showed that the TPC of in vitro digested ripe tomato (61.08 mg gallic acid equivalent (GAE) g−1 sample) was higher than in vitro digested unripe sample (38.97 mg GAE g−1 sample) and that TPC of ripe unprocessed tomato was higher than the processed tomato

  • Higher reducing power was recorded in ripe tomato compared to the processed tomato in both ethanolic extracts and digested samples

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Summary

Introduction

Antioxidants are compounds that help to inhibit many oxidation reactions caused by free radicals, such as superoxide, peroxyl radicals, hydroxyl radicals, nitric oxide and lipid peroxyl, which process, prevents or delays damage to the cells and tissues (Birben, Sahiner, Sackesen, Erzurum, & Kalayci, 2012; Kong & Lin, 2010).Their10.7455/ijfs/9.SI.2020.a3Nutraceutical potential of tomato products after in vitro digestion SI39 mechanisms of action include scavenging of reactive oxygen and nitrogen free radical species; decreasing the localized oxygen concentration, and reducing molecular oxygen’s oxidation potential; metabolizing lipid peroxides to nonradical products; and chelating metal ions to prevent the generation of free radicals (Barzegar, 2012; Madhuri, Qairunnisa, Suresh, Kondam, & Chandrasekhar, 2014). The high content of these compounds in tomato has gained interest due to their apparent multiple biological effects, including free-radical scavenging, metal chelation, inhibition of cellular proliferation, and modulation of enzymatic activity and signal transduction pathways (Vallverdu-Queralt et al, 2011). Lycopene has the capacity to prevent free radical damage to cells caused by reactive oxygen species. Apart from carotenoids, tomato is a source of ascorbic acid, which is an effective scavenger of superoxide, hydrogen peroxide, singlet oxygen and other free radicals (Yafang et al, 2011). The cholinergic hypothesis of Alzhemier’s disease (AD) holds that the degeneration of neurons in the basal forebrain, the associated loss of cholinergic neurotransmission in the cerebral cortex and hippocampus contribute significantly to cognitive deterioration in AD (Craig, Hong, & McDonald, 2011).The loss of cholinergic neurons in AD leads to a reduction in the synthesis of the neurotransmitter, acetylcholine (ACh), which has been associated with cognitive functions.

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