Scientific Basis for Ayurvedic Therapies -18

Scientific Basis for

Ayurvedic Therapies 

edited by

Brahmasree Lakshmi Chandra Mishra

The main symptoms and signs were relieved completely in 3 months, and the patients’

appetites increased. The liver regained normal morphology, jaundice disappeared, blood

pressure became normal, and ascites were not detected. Hepatomegaly and splenomegaly

were reduced. Although the cirrhotic changes in the liver are irreversible, the hepatic functions

can be maintained with the rest of the healthy tissues by this treatment.11

14.6 Liver Cancer

In Ayurveda, tumors are discussed under the names granthi and arbuda to designate basic

common neoplasms, which can appear in any tissue or organ of the body. Granthi, or

minor neoplasm, is a localized small swelling within the subcutaneous fat tissue, muscle,

or blood veins; it is round, erect, and knotted. Arbuda, or major neoplasm, is a spherical,

stable, massive, painless swelling occurring at one site; it expands slowly with deeper

roots. Immobile recurrence of arbuda at the site of previous swelling is called ashyarbuda.

When two arbudas appear simultaneously the condition is known as dvirarbuda, which

indicates their malignant nature.12, 13

The different abnormal growths of pre- and postcancerous states and malignant and

nonmalignant stages arising from various organs are grouped and known as cystic

growths (gulma), benign growths (apaci), lymphatic growths (gandamala), bone tumor

(asthila), cystic tumors (mutragranthi), vaginal tumors (yonikarnini), and systemic tumors

(granthivisarpa and balmika). These growths represent morbid anatomy as neoplasm.13 Both

allopathic and Ayurvedic systems generally refer to neoplasms as the uncoordinated

abnormal cell growth found within particular organs or body tissues.

The words vataja, pittaja, or kaphaja tumors (adenoma) or medhaja (lipoma) or a combination

of any two of them is used to signify a benign neoplasm where one or two of the

three major bodily systems (tridosas) are out of control. Benign tumors are not very harmful

because there is still coordination among the systems, which to some extent controls the

damage. Malignant abnormal growth has been indicated as tridosaja neoplasm (metastatic

tumors), because the three major bodily systems have lost mutual coordination and cannot

prevent damage to tissues, resulting in a deadly morbid condition.13

TABLE 14.6 (continued)

Patent Ayurvedic Formulas for Hepatobiliary Disorders

Formulation, Manufacturer, and Ingredients

Indications

and Dose Ref.

Stimuliv (Fraco-Indian Pharmaceuticals Ltd.)

Kalamegha, Bhringaraja, Parpata, Bhumyamalaki

Viral hepatitis,

hepatomegaly, loss of

appetite, constipation (2

tablets/tsp two times/

day)

83

Vasuliv (Vasu Pharmaceuticals Ltd.)

Bringaraj, Punarnava, Sharapunkha, Kasni, Bjumyamlaki, Kalamegh, Katuki

Liver dysfunction,

hepatomegaly, jaundice,

viral hepatitis, alcoholic

liver diseases (2 tablets

three times/day)

84

According to conventional medical pathology, primary malignant hepatic tumors may

arise from any constituent cells of the liver. Cancer arising from two types of cells are very

common: liver cell cancer (hepatocellular carcinoma) and carcinoma of the biliary epithelium

(cholangiocarcinoma). Other rare tumors that arise from the liver tissue include

fibrolamellar carcinoma, squamous cell carcinoma, epithelial hemangioendothelioma,

angiosarcoma, Kaposi’s sarcoma, hepatoblastoma, and hepatocellular adenoma. In addition

to these malignant primary liver cancers, metastatic involvement of the liver is also

very common because of the extreme chance of spreading cancer from several parts of

the body to the liver.

14.6.1 Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC), also referred to as a fatal malignancy, is regarded as one

of the most aggressive tumors with poor prognosis. It has a worldwide incidence of 250,000

to 1,000,000 patients annually.14 HCC is prevalent in Asia and Africa where annual incidence

of 500 cases occurs per 100,000 population.15 In China, HCC was the third cancer

killer, and annual deaths from HCC have exceeded 110,000, accounting for approximately

45% of the total HCC deaths in the world.16 According to 1996 annual statistics, in the U.S.

there have been more than an estimated 19,500 new cases of HCC and 15,200 deaths due

to this cancer. This estimate is based on incidence rates of the Service, Epidemiology, and

End Results (SEER) program from 1979 to 1992.17

14.6.1.1 Etiology of Liver Cancer

According to Ayurvedic texts, cancer is a disease resulting from the derangement of

bodily systems due to dietary constituents (chemical carcinogenesis). It differs according

to each person’s pathogens (exogenous) and constitutions (genetic, bijadosa).13 Sushruta

called the sixth layer of the skin Rohini (the skin layer with the nature of growth), which

represents the Western medical word epithelium, the layer of cells forming the epidermis

of the skin and the surface layer of the mucous membranes where most cancers originate.

Pathogenic injuries to the inner layer of the dermis can be caused by the imbalances of

three bodily systems or lifestyle errors, such as unhealthy foods, poor hygiene, or

behavioral habits and physical trauma resulting in ulcerous conditions. Because of the

fast-growing nature of these tissues, the process of healing often leaves tiny scars. These

slow-healing ulcers may develop into early neoplasms, which are complicated and

difficult to cure.13

HCC is a multifactorial and multistage process whose precise etiology is not known.

Both chronic hepatitis and cirrhosis are considered major precipitating factors. HBV or

HCV infection results in tumor initiation.14 Other factors include the ingestion of high

amounts of aflatoxins, occupational exposure to vinyl chloride or similar toxic chemicals,

and alcoholism. Long-term use of oral contraceptives and angiogenic therapy have also

been found to cause liver cancer development in fewer cases.

14.6.1.2 Pathogenesis of Liver Cancer

In Ayurveda, Sushruta has proposed six stages of pathogenesis, which apply more to the

neoplasms (especially liver tumors) because of their metastatic nature:

1. Localization of growth (sanchaya)

2. Transformation of growth into metastatic tumors (prakopa)

3. Metastasis (prasara)

4. Secondary growth (sthana samsraya)

5. Expression of symptoms (vyakti)

6. Histopathological differentiation (bheda)

On the basis of tridosas concept, pitta present in each and every cell is responsible for

digestion and metabolic function. In liver cancer, the decreased state of deranged metabolism

(dhatwagni imbalance) results in the excessive growth of the liver tissue and creates

metabolic crisis where anabolic phase exceeds the catabolic phase (aggravation of vatha

forces and suppression of kapha forces) resulting in proliferation. It is clearly stated that

liver enlargement (ekadesavriddhi) is accompanied by weight loss (anyasthaniyakshaya) in

liver cancer.18

14.6.1.3 Diagnosis of Liver Cancer

In early stages, liver cancer usually has no noticeable symptoms. Hepatomegaly (yakrutodara),

with moderate pain (ruk) or tenderness (sparsahsnutwam) that is localized to the

FIGURE 14.1

Ayurvedic description for bilirubin metabolism. (From Mali, M.D. and Kulkarni, P.H., Ayurved and Hepatic

Disorders, Sri Satguru Publications, Delhi, 2001.)

Ayurvedic description for bilirubin metabolism3

Erythrocytes Blood (Rakta)

Macrophages of the spleen

and bone marrow

Excess dosa in blood and pitta (Raktamala pitta)

Heme

Bilirubin

Kidney Bile

Bilrubin conjugate Intestine Intestinal digestion

Urobilin Stercobilinogen Normal stool and urine

THE LIVER Bilirubin

↓

Bilirubin – Albumin

(Unconjugated bilirubin)

↓

Bilirubin diglucoronide

(Conjugated bilirubin)

Toxic pitta (Sampitta)

↓

Metabolism and

detoxification

(Yakrutastha Dhatwagni

kriya)

↓

Non-toxic pitta

(Niram pitta)

Non-toxic pitta (Nirampitta)

upper abdomen or the right upper quadrant, is often the major complaint from the HCC

patients.19 Macroscopically, the tumor may be a solitary mass with multiple necrotic

(kotham) nodules or may present diffusely, which infiltrates the liver and usually is cirrhotic.

On microscopical examination, several abnormal architectural patterns of malignancy

(e.g., trabecular, pseudoglandular, solid, etc.) exist, and these tumors are mitotically

active. In certain cases, abdominal swelling (sopham) due to liver enlargement with or

without ascites also occurs. Pyrexia, pain, or fractures due to bone metastasis are some of

the rare presentations of preneoplastic syndromes. Anorexia (aruchi), weight loss, hypercalcemia,

hypoglycemia, hyperlipidemia, hemotologic, and neurologic syndromes are also

Although serum alpha-fetoprotein (AFP) is a highly specific marker in HCC cases,

ultrasonographic screening is also recommended because AFP levels are not always elevated

in the early stages of HCC (in 30% of cases). Presence of alkaline phosphatase

isoenzymes, carcinoembryonic antigen, and human chorionic gonadotropin are other associated

complications in HCC patients. Bleeding of esophageal varices may present as a

terminal sequele.

14.6.1.4 Treatment

HCC is an important cause of morbidity and mortality worldwide. The course of clinically

apparent disease is rapid, and if untreated, most patients die within 3 to 6 months of

diagnosis. Individual prognostic factors such as the extent of the disease, the site of

metastasis, histological condition of the tumor, and the biochemical abnormalities have

to be considered in selection of a therapy.

14.6.1.4.1 Ayurvedic Treatment Modalities

In Ayurvedic classical texts, specific treatment protocols for liver cancer were not mentioned.

Ayurvedic practitioners are taking the advantage of available knowledge of treatment

on cancer from the old classical texts and are applying those methods in liver cancer

management. Empowerment, participation in the healing process, relief of cancer symptoms,

time and personal attention, and reduced cost of care are essential elements in the

Ayurvedic management of liver cancer.

The fundamental principles of Ayurveda are finding the cause of an illness and restoring

the balance between the three major bodily systems by supplying deficient substances

and by reducing the excessive ones (tridosa siddhanta). Anticancer therapeutic approach

can be divided into four categories:

1. Restoration of balance (prakritisthapani chikitsa)

2. Curative therapy (roganashani chikitsa)

3. Restoration of normal function (rasayana chikitsa) and spiritual therapy (naishthiki

chikitsa)

4. Surgery (considered only as a last resort)

Unlike Western medicine, which mostly epitomizes the one symptom–one disease–one

drug paradigm, Ayurvedic medicines are holistic and go a long way to substantiate the

defects and deficiencies of medical practices.

14.6.1.4.2 General Line of Treatment

1. Purification process (sodhana chikitsa including panchakarma) using internal and

external medications which can eliminate pathogens (dosas)

clinical manifestations that occur during HCC (see Figure 14.1).

2. Curative therapy (samana chikitsa) pacifies pathogens (dosas)

3. Correction of metabolic defects (dhatwagni chikitsa)

4. Immunotherapy (rasayana prayoga)

5. Anticancerous drugs (vyadhipratyanika chikitsa)

6. Symptomatic treatment (lakshanika chikitsa)

7. Surgical treatment with herbal and mineral medicines (Sastra chikitsa)18

The herbal treasure chest of ancient Ayurveda offers a host of new phytochemicals that

can be used both preventively and clinically to manage a spectrum of liver-related imbaleffective

therapies for liver diseases, but also their underlying scientific principles based

on an extensive literature search of Ayurvedic texts and research reports on hepatoprotective

herbs with anticancerous property. Ayurvedic practitioners are using Ayurvedic

Many Ayurvedic drug manufacturers are designing their own appropriate drug formuladients;

these agents may operate synergistically, producing tremendous therapeutic

benefits, lowering risks on adverse effects, and avoiding unnecessary supplemental therapy.

The benefit of an herbal formula is that it can nourish the body as a whole by

supporting various organ systems, yet its main focus will be on nourishing the liver and

its functions. These formulations are reported to work on multiple biochemical pathways

and are capable of influencing several organ systems simultaneously. This kind of orientation

makes the Ayurvedic approach to liver cancer especially attractive.

14.6.1.4.3 Allopathic Treatment

Among allopathic treatment modalities, surgery is seldom of value for hepatic metastases

nor is hormonal therapy. In radiotherapy using intraarterial 131iodine-lipiodol20 or

90yttrium, microspheres,21 the clinical benefits are of modest value because of side effects

like fibrosis, pneumonitis, neurological abnormalities, colitis, enteritis, malabsorption, and

sterility. Although chemotherapy is an essential component of an effective multidisciplinary

cancer treatment program, current systematic therapies with 5-fluorouracil, floxuridine,

doxorubicin, mitomycin-C, and cisplatin are less effective and responses are

partial (5 to 25% range) and short lived.22

Radiotherapy and chemotherapy also damage adjacent healthy cells and increase the

possibility of developing a secondary cancer; many times, the mortality increases by the

toxicity of the drug or radiation rather than the disease. Other approaches, namely, hepatic

artery embolization with chemotherapy, alcohol ablation, ultrasound guided cryoablation,

immunotherapy with monoclonal antibodies, and gene therapy with retroviral vectors,

are also of only minimal benefit. Liver transplantation may be considered as another

therapeutic option, but again the recurrence of tumor or metastases after transplantation

has limited its usefulness. The major drawback with the treatment of HCC is that it has

a significant propensity to develop metastases with major sites spreading to other parts

of the liver, lymph nodes, lungs, bones, adrenal glands, and the peritoneal cavity.23 Multifocal

HCC is a very difficult neoplasm to treat due to the lack of efficacy of chemotherapeutic

regimes and the inaccessibility of this tumor to surgical procedures. The World

Health Organization (WHO) also categorized hepatic cancers under group 3 tumor, for

which there are no effective drugs.24

ances, including hepatocarcinoma. Tables 14.2 and 14.3 describes not only efficient and

text preparations that utilize the recent research outcomes on anticancer herbs (Table 14.5).

tions (Table 14.6). These herbal formulas contain multiple chemical agents as active ingre-

Given the lack of useful therapies for this disease, there is a great need to discover

drugs that are selectively cytotoxic only to hepatic cancer cells without damaging the

body’s other normal cells. Because Ayurvedic herbal therapies have the potential to

inhibit cancer cells without damaging normal cells, liver cancer patients who already

are crippled with the disease and burdened by chemotherapy-induced toxic side effects

are often turning to seek help from Ayurvedic physicians. Patients hope for a better cure

without adverse side reactions from Ayurvedic therapies. The high cost of conventional

medicine is also driving the search for alternatives in other medical systems such as

Ayurveda.

14.7 Prevention of Hepatic Diseases

Prevention is a preferred strategy than cure, especially for chronic hepatic diseases such

as liver cancer. Regular intake of hepatoprotective herbal tonics would be beneficial in

this strategy. It may also be argued reasonably that prevention of viral infection by HBV

vaccine may help prevent HCC. The antifibrotic agents prolyl 4-hydroxylase inhibitor

(HOE 077), sho-saiko-to (TJ-9), and interferon can also reduce the risk of development of

HCC.25

14.8 Scientific Basis

14.8.1 Phyllanthus niruri/amarus (Bhumyamalaki)

14.8.1.1 Clinical Trials

In a clinical study26 conducted on 55 patients with chronic viral hepatitis, all the 30

patients under P. amarus treatment were cured within 3 months with remarkable recovery

of liver functions and inhibition of HBV replication. Another study27 indicated that 59%

of the P. amarus-treated patients became HBAg negative.

14.8.1.2 In Vivo and In Vitro Studies

The aqueous extract of P. amarus not only increased the life span of the N-nitrosodiethylamine-

induced HCC-bearing rats from 33 to 52 weeks, but also normalized gamma

glutamyl transpeptidase and serum HCC marker activity.28 The ethanolic extract exhibited

a hepatoprotective effect on alcohol toxicity in rats and in carbon tetrachloride and galactosamine-

induced cytotoxicity in primary cultured rat hepatocytes.29 P. amarus extract

inhibited HBAg secretion in Alexander, a human hepatocellular carcinoma cell line,

because of its ability to down-regulate HBV messenger ribonucleic acid (mRNA) transcription

and up-regulate HBV enhancer I activity.30 It also inhibited HBV polymerase

activity and decreased episomal HBV DNA content.31

14.8.2 Picrorrhiza kurroa (Katuki)

14.8.2.1 Clinical Trials

The active principle of katuki is kutkin. The standardized preparation used in studies is

Picroliv. In a placebo-controlled trial32 with acute viral hepatitis patients, P. kurroa (375 mg

three times/day for 14 days) normalized liver function test (LFT) parameters with quicker

clinical recovery and 100% clinical and biochemical clearance.

14.8.2.2 In Vivo and In Vitro Studies

P. kurroa acts as a direct viricidal agent and alters biotransformation of the toxins. In several

studies33,34 it inhibited the uncoupling between respiration and oxidative phosphorylation

and aflatoxin-induced lipid peroxidation in rats. In addition, it caused the reversal of lowdensity

lipoprotein binding to paracetamol and lowered bilirubin level by biliary flow

stimulation. It also showed a protective role against ethanol and carbon tetrachlorideinduced

toxicity in rat hepatocytes.35 During Plasmodium berghei infection in Mastomys

caucha, it showed hypolipidemic property by regulating lipolytic enzymes.36 As an effective

inhibitor of hepatocarcinogenesis, it normalized liver function enzymes and reduced liver

enlargement and hepatic nodular formation in N-nitrosodiethylamine-induced hepatocarcinoma

conditions.37

14.8.3 Podophyllum hexandrum Linn. (Giriparpata, Vanatrapusi)

14.8.3.1 Clinical Studies

P. hexandrum (active constituent: Podophyllotoxin) is a hepatic stimulant, blood purifier,

and raktaarbudanasna (anticancer drug). Etoposide (VP-16), a semisynthetic derivative of

podophyllotoxin, has been used against HCC for several years. P-glycoprotein, an energydependent

drug efflux pump that reduces intracellular concentration of drugs in tumor

cells, seems to be less effective in reducing VP-16 concentration in hepatoma cell lines;

this drug is found to be more efficient in hepatocarcinoma.38 In a phase II study on

anticancer effectiveness of VP-16 in combination with epirubicin, 3% of 36 HCC patients

achieved complete response, 36% had partial response, and 31% exhibited stable disease;

the disease progressed in another 31% of patients.39

14.8.3.2 In Vivo and In Vitro Studies

P. hexandrum has the property of karyoplastic and causes mitotic arrest, nuclear fragmentation,

and impaired spindle formation dispersing the chromosomes. Necrosis and rapid

reduction of the cytochrome oxidase are suggested mechanisms for its antitumor property.40

14.8.4 Tinospora cordifolia (Guduchi)

14.8.4.1 Clinical Trials

In a study41 with malignant obstructive jaundice patients, T. cordifolia decreased morbidity

and mortality due to liver cell failure. In addition, a 92.4% survival rate after treatment

without blood poisoning was noticed when compared with only a 40% survival rate on

conventional treatment. As an immunomodulator, it strengthened host defense and normalized

phagocytic and killing capacities of neutrophils. In another study42 with hepatitis

patients, the treatment showed symptomatic relief with improvement in yellow discoloration

of urine and body and reduction of LFT parameters. Of a total of 20 cases, 75% were

cured and 25% improved from their illness.

14.8.4.2 In Vivo and In Vitro Studies

T. cordifolia prevented fibrosis by hepatic tissue regeneration, membrane stabilization, and

activation of kupffer cells in carbon tetrachloride-induced liver damage in rats.43 In experimental

animal tumors, it increased IgG antibodies and enhanced humoral- and cellmediated

immunity.44 It not only stimulated the proliferation of stem cells and increased

white blood and bone marrow cells, but also reduced tumor volume by 58.8%, which was

comparable with cyclophosphamide.45

14.9 Summary and Conclusion

The complete cure of liver diseases such as HCC is one of the biggest challenges in the

medical world. Scientific researchers in medical sciences are conducting multidirectional

research on various aspects of hepatic disorders in order to determine useful remedies for

these dreadful diseases. New findings discussed are a result of the development of

Ayurvedic science through the ages and their accomplishments in modern cancer therapeutics.

The details of experimental and clinical studies conducted on single and compound

Ayurvedic preparations for their efficacy against liver cancer and other hepatic

ailments are also important; they strongly emphasize Ayurvedic therapy as a scientifically

feasible medical practice and an unconventional entity. Research in this field should be

sustained and strengthened in order to better understand its scientific merit and determine

its utility for a heterogenous population. Hepatic diseases are no longer inevitable and

can be prevented and effectively treated. Ayurvedic medicine now has an opportunity to

contribute to the end of liver cancer’s long scourge of mankind.

Acknowledgments

The authors are highly thankful to the authorities and staff of the literary research and

documentation department, Central Research Institute (Siddha), Chennai, India for permitting

the use of their library facilities.

Scientific basis for other hepatoprotective Ayurvedic herbs are continued in Table 14.3.

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Antimutagenic Effect of Ayurvedic Therapies

Satwinderjeet Kaur

15.1 Introduction

The purpose of this article is to explore the antimutagenic effect of Ayurvedic therapies,

as this effect may be an underlying mechanism of their therapeutic uses. Also, these

products may act to supplement antimutagens in our diets which have now become

essential in order to combat the unavoidable environmental mutagens to which we are

constantly exposed.

15.2 Background

A technologically advanced society creates an environment that warrants exposure to

different types of genotoxic substances. The deoxyribonucleic acid (DNA) from living

organisms is continuously exposed to exogenous or endogenous damaging agents as a

result of which there is a substantial level of DNA damage. It has been hypothesized that

DNA damage contributes to organismal senescence and the increased risk for specific agerelated

diseases.

1–4

DNA lesions can interfere with most DNA metabolisms, including

replication, transcription, and recombination as well as other important cell functions (e.g.,

cell-cycle regulation or cell division). Cancer initiation is classically associated with the

induction of mutations on specific oncogenes or tumor suppressor genes due to the

presence of unrepaired DNA lesions produced by endogenous or exogenous genotoxic

agents. The somatic mutation theory proposes that changes in DNA are responsible for

changes that bring about senescence and death.

Exposure to mutagens and carcinogens either endogenously or exogenously is unavoidable.

Cigarette smoking, diet, infection, and chronic inflammation account for a large

proportion of cancers. Epidemiological studies have indicated that cigarette smoking

significantly elevates the risk of tumor development in the upper-aerodigestive tract and

in other organs.

5,6

Polycyclic aromatic hydrocarbons, N-nitrosamines, and many mutagens

and carcinogens and their precursors have been detected from cigarette smoke condensate.

5,6

The total calorie intake and fat intake appear strongly associated with enhancement

of human cancer development.

7–10

Lipid peroxidation yields exocyclic propano-, etheno-,

and malondialdehyde adducts in DNA to induce mutation.

11,12

The mutagens and carcinogens

may be present as microcomponents in various foodstuffs.

13,14

The compounds

include naturally occurring pyrrolizidine alkaloids, ptaquiloside, and cyasin. Mycotoxins

like aflatoxin B

1

, sterigmatocystin, and fumonisin exist as contaminants in food. Hepatocarcinomas

developed in people who are living in areas where alfatoxin B

1

is highly

contaminated in diet show a characteristic mutation in the p53 gene, namely, change of

G to T at the third position of codon 249.

15,16

It is practically difficult to completely eliminate mycotoxin contamination of food materials.

Heterocyclic amines (HCAs) are produced under normal cooking conditions, especially

in the overcooked fish and meat. HCAs are metabolized by the cytochrome P450

family, especially by CYP1A2 to

N

-hydroxyamino derivatives, and are then esterified to

the ultimate forms that produce DNA base adducts.

17,18

Infection and chronic inflammation

may produce oxidative agents in addition to cytokines and chemokines that enhance cell

proliferation, increasing the chance of replication error and genetic change.

15.3 Mechanism of Mutagenic Activity

The generation of reactive oxygen species (ROS) in biological systems, either by normal

metabolic pathways or as a consequence of exposure to chemical carcinogens, has been

extensively studied.

19

Free radicals generate oxidative damage to main cellular components

such as DNA, lipids, carbohydrates, and proteins; they have been implicated in the

aging phenomena, ischemia,

20

cancer,

21

autoimmune diseases,

22

and neural cell death.

23

It

is now universally agreed that the ROS generation contributes to the multistage process

of carcinogenesis.

19,24

Evidence has accumulated that lack of protection against free-radicals

and lack of repair of oxidative damage in biological macromolecules have a significant

role in mutagenesis and carcinogenesis. Kawanishi and co-workers

25

reported that

sequence-specific oxidative damage to DNA may play an important role not only in

carcinogenesis but also in aging.

15.4 Prevention

There are two complementary strategies for preventing chronic degenerative diseases. The

first one is avoidance of exposure to recognized risk factors which evolves through risk

assessment and risk management. The risk management is based either on risk communication

and health education for controlling lifestyle risk factors or on suitable regulations

for controlling environmental risk factors. The other strategy is to favor the intake of

protective factors and to modulate the host defense mechanisms. This approach is more

practical and is referred to as chemoprevention. It is based on dietary and pharmacological

interventions, has already found extensive application in the field of cardiovascular disease,

and is encountering a growing interest in cancer prevention.

Food is a complex mixture that may contain mutagenic or carcinogenic compounds such

as polycyclic aromatic hydrocarbons and heterocyclic amines present in meat.

26,27

On the

other hand, food may contain protective antimutagenic or anticarcinogenic substances

that are mostly present in plants. It is important to maintain a varied nutritionally balanced

diet in which food antimutagens outweigh the mutagens. Inhibition of mutagenesis or

carcinogenesis is generally not based on one mechanism. Protection against cancer can

occur at different stages of the complicated processes of carcinogenesis. Compounds and

complex mixtures with antimutagenic activity have different modes of action and act in

parallel at different levels. As inhibitors, they may prevent the formation of mutagens,

such as the endogenous formation of nitrosamines. As blocking agents, they can prevent

the biotransformation of promutagens into reactive metabolites by inhibiting metabolic

activation, stimulating detoxification enzymes, or scavenging reactive molecules. As suppressing

agents, they may modulate intracellular processes, which are involved in DNA

repair mechanisms, tumor promotion, and tumor progression.

28

Discovery and exploration

of compounds possessing antimutagenic and anticarcinogenic properties are of great

importance.

Om Tat Sat

                                                        

(Continued...) 

(My humble salutations to H H Maharshi ji,  Brahmasri Sreeman Lakshmi Chandra Mishra ji and other eminent medical scholars and doctors   for the collection)