The antioxidant properties of tea are the major hypothesis of its beneficial health effects. The polyphenols reaction mechanism can proceed in two ways, first one is transfer of hydrogen atom and the second is transfer of single electron.

By Hafiza Arooj Kanwal1, Wafa Majeed1, Bilal Aslam1, Ambreen Mehmood1

Antioxidant and antiradical effect

Green tea has the potential to donate hydrogen atoms to free radicals due to ­hydroxyl groups of polyphenols (catechins and gallic acid). Oxidation processes like the hydrogen peroxide, oxide radical anion, hydrogen peroxide radical, hydroxyl radical as well as singlet oxygen and ozone are the most dangerous forms.  Catechins and gallic acid are compulsory to make health better. Processes of oxidation occur by many mechanisms; therefore, it is very important to examine their reaction with aggressive polyphenols and forms of oxygen. Unstable forms of hydroperoxides can also be reduced, scavenged or deactivated by their usage.

Anti-mutagenic and anti-carcinogenic potential

Several steps have been proposed in the process of carcinogenesis named as `multi-step carcinogenesis’ given in Fig. 1. The schematic conversions of normal cells to tumor cells which proceed cancers. Initiation involves the mutation in genes of DNA chromosomes that is first step. In the second step, the abnormal proliferation happens in abnormal style to make enzyme active and alter metabolism in cells, it is called ‘promotion’. The third step in which tumor cells grow faster than normal cells and do attack on them, is called `progression’.


Fig. 1: Multistep carcinogenesis and its inhibition by tea polyphenols.

At different stages of carcinogenesis, mutagenesis, invasion and metastasis of tumor cells, tea polyphenols produce their inhibitory actions due to various mechanisms. In Table 1, classification of the mechanisms of anti-mutagenesis and anti-carcinogenesis of tea polyphenols is shown. They act intracellularly as bio-antimutagens and extracellularly as desmutagens inhibit the promotion of initiated cells and the metastasis of tumor cells.

Inhibitors of mutagenesis and carcinogenesis help to balance or regulate the cascade of occasions engaged with the consecutive steps, which prompting mutations and tumors. At various phases of mutagenesis, cancer and metastasis of tumor cells, tea polyphenols produce their inhibitory activities because of different components. In Table 1, green tea polyphenols are classified according to the anti-mutagenic and anti-carcinogenic mechanism of action. They act intracellularly as bio-antimutagens and extracellularly as desmutagens restrain the advancement of new cells and provoke the metastasis of malignant cells.


Table 1: Mode of action of green tea polyphenols (catechins) against mutagens and carcinogens


Tea polyphenols

Mechanisms of carcinogenesis

1. Desmutagenesis (extracellularly blockade of mutagens and carcinogens)

Extract of green tea

Interact with MNNG

2. Bio-anti-mutagenesis (intracellularly blockade of mutagens and carcinogens)



2.1Modulation of metabolism

Green tea

Prohibition  of cytochrome P-450-dependent metabolic activation

a. Inactivation of promutagens

Catechins (polyphenols)

Blockade of the S9 enzymes


Extract of green tea

Interact with promutagens

b. Detoxifying mechanism activated

Green tea

Glutathione induction



Propagation  of phase II Enzymes

c. Detoxification due to alteration in metabolic enzymes

Green tea

Decrease in cyto P450 and elevate enzymes of phase II

2.2 Suppression or inhibition



a. Reactive molecules inactivation


Suppression or inhibition

b. ROS scavenging activity


Down regulation of hydroxyl radicals



Inhibition of DNA cleavage


Polyphenols of green tea

Antioxidant effects



Cessation of catalytic cytochrome P-450

2.3 Propagation of DNA replication



a. DNA replication fidelity elevated


Interact with DNA polymerase III

b. DNA repair


Excision-repair system updated

3. Block initiation  of neoplastic cells


Tumor promotion cession

4. Blockade of invasion and metastasis


Block matrix enzymes


Extract of green tea

Block matrix enzymes



Block urokinase

5. Apoptosis


DNA fragmentation formation




Effect on lipid

Hyperlipidemia is one of the significant danger factors for the advancement of fatty liver which results from the anomalies of lipid digestion. The expanded plasma lipids, for example, phospholipids, fatty acids, cholesterol and fatty substances can prompt the advancement of atherosclerotic plaques. The danger of fatty liver diminished by 2% with a 1% decline in serum cholesterol. Green tea polyphenols (catechins) forestall the presence of atherosclerotic plaque in different models of hyperlipidemia and influence lipid digestion by different systems. Moreover, catechins impact luminal lipid hydrolysis, micellular dissolvability and intestinal lipid retention and up-control hepatic LDL receptor articulation, in this manner regulating biosynthesis, discharge and intracellular preparing of lipids. This might be because of a decrease of cholesterol focus in liver, given that diminished intracellular cholesterol levels increment LDL receptor combination. Catechins may meddle with lipids through hydrolysis, emulsification and solubilization.

Anti-inflammatory effect

Chemotactic cytokines and vascular grip particles direct the bond of leukocytes to ECs fundamentally. Chemokine interleukin-8 and monocyte chemoattractant protein-1 are discovered to be the focal factors in monocyte enlistment into sub-endothelial sore in liver damage. Grip atoms like endothelial leukocyte attachment particle, intercellular bond particle and vascular attachment particle controlled by NF-kB, assume a critical function in pulling in authoritative and immigration of leukocytes into locales of inflammation. Catechins can restrain leukocyte-endothelial association as indicated by In vitro investigations. It is an impact reliant on the bunch in catechins since ECG, EGC and EC were unaffected by it. ECs and along these lines diminish the movement of monocyte cells, an impact propagated via synergistic effect of p38 mitogen-enacted protein kinase and NF-kB activation. EGCG likewise repress neutrophil relocation through refined human endothelial monolayers at physiological reachable focus. ECG and EGCG likewise initiate caspase-mediated apoptosis of monocytes and stifle bothersome resistant reaction and resultantly assume a key function in atherogenesis. It additionally stifles chemokine creation and neutrophil infiltration at the inflammatory site.

Anti-obesity effect of green tea

GTC impact body weight, thusly, body arrangement stays a functioning territory of examination. The impacts of GTC on thermogenesis and substrate oxidation are centered fundamentally in people, both are intervened by sympathetic nervous system movement. Other potential components remember changes for hunger control, diminished supplement assimilation and down-guideline of chemicals engaged with hepatic lipid metabolism. Proof for every one of these indicated instruments will be introduced (Fig. 2).

Fig. 2: Anti-obesity mechanism of green tea.

The sympathetic nervous system (SNS) assumes a critical part in the guideline of energy consumption and lipolysis of Norepinephrine (NE) is a key middle person of SNS action, substances that invigorate its essence bring about increment energy use and advance the oxidation of fat. In 1975, Borchardt and Huber gave proof that GTC represses catechol O-methyltransferase (COMT). COMT is a catalyst that debases norepinephrine and delay the activity of sympathetically delivered NE in the synaptic split.

The impact of lifestyle changes on diet

Intake of calorically rich diets combined with chronic over-nutrition and a sedentary lifestyle evokes a condition of chronic metabolic inflammation, called meta-flammation. Meta-flammation leads to the production of many prevalent non-communicable diseases (NCDs), and with global epidemic dimensions, these lifestyle-associated pathologies pose a growing public health concern. For the creation of successful preventive and therapeutic strategies for common NCDs, a better understanding of how modern lifestyles and diets (WD) stimulate immune cells is necessary.

In obese individuals, an overflow of 1000 kcal for 12 weeks, prompting a weight put on of 6 percent body weight, increments intrahepatic liver (IHL) proximately 50 percent, through expanded de novo lipogenesis alongside decreased oxidation of intrahepatic fatty acids, while the accessibility of fatty acids is less significant in this setting. An oral saturated fat intake expands IHL, decreases human affectability to hepatic insulin, and causes an inflammatory phenotype and independent of body weight, in rats. In any case, insulin-resistant people suffer with steady weight reduction through low calories diet (50-57 percent of energy as sugar, around 29% fat, and 16-20 percent protein) continuously decreases IHL. The impact is intervened in any event to some extent by decreased accessibility of fatty acids through expanded affectability to insulin in adipose tissue. Fatty liver index is an indicator calculation for fatty liver disorders, which was dependent on BMI parameters, waist outline, triglycerides and GGT. In this calculation, FLI scores under 30 consider safe that avoid fatty liver, scores under 30 and 60 stay uncertain. Scores of 60 or more show that fatty liver is diagnosed.


Hafiza Arooj Kanwal1, Wafa Majeed1, Bilal Aslam1, Ambreen Mehmood1

1Institute of Pharmacy, Physiology and Pharmacology, University of Agriculture, Faisalabad, Pakistan.