Study on phytochemical profile and anti-ulcerogenic effect of cayratia pedatata lam in albino wistar rats

Abstract

The aim of this study is to evaluate the anti-ulcer activity of chloroform extract of leaves of Cayratia pedata (Lam). The chloroform extract of Cayratia pedata (CECP) was investigated for its anti-ulcer activity against pylorus ligation and ethanol induced gastric ulcers in rats. Ranitidine (50mg/kg,p.o.) and misoprostol (100ug/kg,p.o.) were used as standard drugs. A significant (p<0.01) anti-ulcer activity was observed in both the models. Both does of Cayratia pedata produced gastric anti-secretory effect in pylorus ligated rats and also showed gastric cytoprotective effect in ethanol induced gastric ulcers. Pylorus ligation showed significant (p<0.01) reduction in gastric volume. Free acidity, ulcer index as compared to control. It also showed significant (p<0.01) reduction in ulcer index in ethanol induced model with respect to control. This present study indicates that, Cayratia pedata leaves extract have potential anti-ulcer activity in this tested models.

Full text

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Study on phytochemical profile and anti-ulcerogenic effect of Cayratia pedatata Lam
in albino wistar rats
*P.Karthik, 1P.Amudha, 2J.Srikanth
*,1Asst. Professor, Department of Pharmacology, C.L.Baid Metha College of Pharmacy, Thorapakkam,
Chennai, Tamil Nadu.
2Faculty of Pharmacy, Sri Ramachandra University, Chennai, Tamil Nadu.
Summary
The aim of this study is to evaluate the anti-ulcer activity of chloroform extract of leaves of
Cayratia pedata (Lam). The chloroform extract of Cayratia pedata (CECP) was investigated for
its anti-ulcer activity against pylorus ligation and ethanol induced gastric ulcers in rats.
Ranitidine (50mg/kg,p.o.) and misoprostol (100ug/kg,p.o.) were used as standard drugs. A
significant (p<0.01) anti-ulcer activity was observed in both the models. Both does of Cayratia
pedata produced gastric anti-secretory effect in pylorus ligated rats and also showed gastric
cytoprotective effect in ethanol induced gastric ulcers. Pylorus ligation showed significant
(p<0.01) reduction in gastric volume. Free acidity, ulcer index as compared to control. It also
showed significant (p<0.01) reduction in ulcer index in ethanol induced model with respect to
control. This present study indicates that, Cayratia pedata leaves extract have potential anti-ulcer
activity in this tested models.
Keywords: Cayratia pedata (Lam), Pylorus Ligation, Ethanol Induced Gastric Ulcers.
*P.KARTHIK M.Pharm.,
Department of Pharmacology,
C.L.Baid Metha College of Pharmacy,
Thorapakkam, Chennai, Tamil Nadu
E mail: karthikram_2004@yahoo.co.in
Introduction
Peptic ulcer disease (encompassing gastric ulcer and duodenal ulcer) affect a large portion of the
world population and are induced by several factors, including stress, smoking, nutritional
deficiencies, and ingestion of non-steroidal anti-inflammatory drugs [1]. The pathophysiology of
these ulcers involves an imbalance between offensive (acid, pepsin, and Helicobacter pylori) and
defensive factors (mucin, prostaglandin, bicarbonate, nitric oxide and growth factors). Today,
there are two main approaches for treating peptic ulcer. The first deals with reducing the
production of gastric acid and the second with re-enforcing gastric mucosal protection [2,3]. There
has been a rapid progress in the understanding of the pathogenesis of peptic ulcer. Modern
approach to this includes proton pump inhibitors, histamine receptor blockers, drugs affecting the
mucosal barrier and prostaglandin analog [4]. Development of tolerance and incidence of relapses
and side effects on clinical evaluation make their efficacy arguable. This has been the basis for the
development of new antiulcer drugs, which includes herbal drugs.

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Cayratia pedatata lam (Family- Vitaceae) Endemic to southern western ghats in Kerala
and Tamil Nadu. In Kerala, reported only from Palakkad forest in Silent Valley, where it is
locally common. In Tamil Nadu, collected only from Nilgiris. It may possibly occur in the high
ranges of Anamalais and Kodaikanal hills [5,6]. In folklore claim, it is used for treating diarrhea,
burns, refrigerant, ulcers, uterine, flukes, hysteria (India) Astringent, [5,7], uterine reflexes (Sri
Lanka) low diuretic activity and has been a reputed remedy for cough, bronchitis, asthma, joint
pain and to check uterine reflexes [7,8]. From the source of literature documentation and relevant
traditional approaches on plant drugs, the present investigation was carried out to investigate the
constituents and anti-ulcer profile of the chloroform extract of Cayratia pedatata lam (CECP) is
being reported here.
Materials and Methods
Collection and authentication of plant material
The leaves of Cayratia pedata lam were collected from the Palakadu forest in Kerala, in the
month of September. The plant material was identified and authenticated by Mr. Chelladurai,
Research officer- Botany, C.C.R.A.S. Govt of India, Tirunelveli. The voucher specimen of the
plant was deposited in the college for further references.
Preparation of plant extract
Freshly collected leaves of Cayratia pedata lam were dried to get a coarse powder. A
weighed quantity of the powder was passed through sieve number 40 and extracted using soxhlet
apparatus with chloroform as a solvent at a temperature range of 60OC47. The extract was
concentrated by distilling off the chloroform and then evaporating to dryness on a water bath.
Before and after every extraction the powder bed was completely dried and weighed. The
percentage yield of chloroform extract was 18.4%W/W. The chloroform extract was administered
to the animals by suspending each time in 1% CMC.
Phytochemical Screening
The phytochemical examination of chloroform extract of Cayratia pedatata lam was performed by the
standard methods [9].
Experimental animals
Adult Wistar rats of either sex weighing 180-250 gms were used in pharmacological and
toxicological studies. The inbred animals were taken from the animal house in C.L.Baid Metha
College of Pharmacy, Thoraipakkam, Chennai-97. The animals were maintained in a well
ventilated room with at 12:12 hr light, dark cycle in polypropylene cages and maintained at
22±1˚C with humidity at 55±5%. They were fed balanced rodent pellet diet from Poultry
Research station, Nandanam, Chennai-35 and tap water ad libitum throughout the experimental
period. The experimental protocol was approved by the Institutional Animal Ethics Committee
(IAEC) of CPCSEA (Committee for the Purpose of Control and Supervision of Experimental
Animals). (Regd.No.930/a/06/CPCSEA. Dt. 30-06-2006.
Acute toxicity study
The acute toxicity of chloroform extract of Cayratia pedatata lam leaves was determined as per
the OECD guideline no. 423 (Acute Toxic Class Method). It was observed that the test extract
was not lethal to the rats even at 2000mg/kg dose. Hence, 1/10th (200mg/kg) and 1/5th (400mg/kg)
of this dose were selected for further study [10].

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ANTIULCER ACTIVITY
Pylorus ligated model
Wistar rats of either sex weighing 180 to 250 g were divided into five groups of six
animals each.
GROUP I Control animals which are pretreated with suspended 1% CMC, ml/100g.
GROUP II Pylorus ligated animals which are pretreated with 1% W/V CMC, 1ml/100g.
GROUP III Pylorus ligated animals which are pretreated with CECP (200mg/kg p.o) suspended
in 1%w/v CMC.
GROUP IV Pylorus ligated animals which are pretreated with CECP (400mg/kg p.o) suspended
in 1%w/v CMC.
GROUP V Pylorus ligated animals which are pretreated with Ranitidine (50mg/kg, p.o)
suspended in 1%w/v CMC.
PROCEDURE
Groups III and IV animals were treated with CECP and group V were treated with
ranitidine for the respective 5 days daily. On day 6th after the last dose, all the groups were kept
for 18h fasting and care was taken to avoid coprophagy [11]. Animals were anaesthetized using
ether the abdomen was opened and pylorus ligation was done without causing any damage to its
blood supply. The stomach was replaced carefully in the abdomen and the wound was sutured by
interrupted sutures. After 6 hr53, stomachs were dissected out and cut open along the greater
curvature and the content were drained into small beakers, centrifuged and then subjected to
analysis for gastric volume, free acid, total acid and protein estimation [12]. The mucosa was
flushed with saline and the stomach was pinned on frog board and the ulcer score was
calculated.
Ethanol Induced Ulcer
Wistar rats of either sex weighing 180 to 250 g were divided into five groups of six
animals each.
GROUP I Control animals which are pretreated with suspended 1% CMC, 1ml/100g.
GROUP II Ethanol (1ml/200g p.o) induced ulcer which are pretreated with 1% W/V CMC,
1ml/100g.
GROUP III Ethanol (1ml/200g p.o) induced ulcer which are pretreated with CECP (200mg/kg
/p.o) suspended in 1%w/v CMC.
GROUP IV Ethanol (1ml/200g p.o) induced ulcer which are pretreated with CECP
(400mg/kg /p.o) suspended in 1%w/v CMC.

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GROUP V Ethanol (1ml/200g p.o) induced ulcer which are pretreated with Ranitidine
(50mg/kg/p.o) suspended in 1%w/v CMC.
Procedure
Groups III and IV animals were treated with CCEP and group V animals were treated
with ranitidine for the respective 14 days. On day 15th after the last dose, all the groups were
kept for 24h fasting and care was taken to avoid coprophagy56. The 100 % ethanol (1ml/200g
p.o) was administered to the groups II, III, IV and V animals and after 1 h animals were
sacrificed by cervical dislocation and stomachs were dissected out and cut open along the greater
Curvature and examined for ulcer [13].
Measurement of ulcer index
The stomachs were excised and were examined for hemorrhagic lesions in glandular mucosa.
Immediately after the animals were sacrificed, their stomachs were dissected out, cut along the
greater curvature and the mucosa were rinsed with cold normal saline to remove blood
contaminant, if any. The sum of the length (mm) of all lesions for each stomach was used as the
ulcer index (UI), and the percentage of inhibition (%I) was calculated as described by Nguelefack
et al. [14] using the following formula:
(USc − USt)
%I = ---------------------------× 100
USc
Where USc = ulcer surface area in control and USt = ulcer surface area in treated animals.
Histological examination
Two animals from each group were sacrificed and the stomach was isolated, washed
with saline and preserved in 10% formalin for histopathological studies. The sections of the
stomach, stained with hematoxylin and eosin, were assessed for histopathological changes such
as congestion, edema, hemorrhage and necrosis. Histological measurement and photographs
were taken (magnification 100 X).
BIOCHEMICAL ESTIMATIONS
Pylorus ligated model
Determination of gastric volume
After sacrificing the rat, the stomach portion was removed. The gastric contents were
transferred in to the centrifuge tube, and centrifuged at 1000 rpm for 10 minutes. The supernatant
liquid was then transferred to a measuring cylinder, and the volume was measured.
Determination of pH of gastric content
1 ml of the gastric juice was collected, and pH was directly measured by using pH strip[15].
Determination of free acidity and total acidity
The total volume of gastric content was measured. The gastric contents were centrifuged
and filtered. One ml of the gastric juice was pipetted out and the solution was titrated against 0.1N
sodium hydroxide using 2 to 3 drops of Topfer’s reagent as indicator, to the endpoint when the
solution turned to yellowish orange colour was observed. This indicated the volume of NaOH
required neutralizing the free hydrochloric acid present in the gastric juice. Then 2 to 3 drops of
phenolphthalein solution was added and titration was continued until a definite red tinge

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reappears. The difference between the two readings indicated the volume of NaOH required
neutralizing the combined acid present in the gastric juice. The sum of the two titrations was the
total acid present in the gastric juice [16].
Acidity was calculated by using formula;
Vol. of NaOH X Normality of NaOH
Acidity = _____________________________________ m. Eq. /dl.
Vol. of Gastric juice used
Estimation of total proteins
Reagents
Alkaline copper reagent
Solution A: 2% sodium carbonate in 0.1N sodium hydroxide
Solution B: 0.5% copper sulphate in 1% sodium potassium tartarate. 50 ml of solution A was
mixed with 1 ml of solution B just before use. Folins phenol reagent. One volume of folins
reagent was diluted with two volumes of distilled water just before use.
Standard bovine serum albumin
20 mg of bovine serum albumin was dissolved in 100 ml of distilled water. Few drops of NaOH
was added to it aid complete dissolution of bovine serum albumin and to avoid frothing, it was
allowed to stand overnight in a refrigerator.
Procedure
The dissolved proteins in gastric juice were estimated in the alcoholic precipitate obtained
by adding 90 % of alcohol with gastric juice in 9: 1 ratio respectively. Then 0.1 ml of alcoholic
precipitate of gastric juice was dissolved in 1 ml of 0.1 N NaOH and from this 0.05 ml was taken
in another test tube. To this 4 ml of alkaline copper reagent was added and kept for 10 minutes.
Then 0.5 ml of phenol reagent was added and again 10 minutes was allowed for color
development. Reading was taken against blank prepared with distilled water at 640 nm. The
protein content was calculated from standard curve prepared with bovine albumin and has been
expressed in terms of µg/ ml of gastric juice [17].
Statistical Analysis
The data represents Mean ± SEM. Results were analyzed statistically using one way
ANOVA followed by Dunnet’s ‘t’ test. The minimum level of significance was set at (P<0.05).
Results
Phytochemical investigation
The results of preliminary phytochemical investigation of the chloroform extract of Cayratia
pedatata lam leaves (CECP) shows the presence of carbohydrates, steroids, sterols, phenols,
flavanoids, glycosides, terpenes and absence of alkaloids, tannins, gum and mucilage and
Saponins.
Acute toxicity study
Acute toxicity study in which the animals treated with the CECP at a higher dose of 2000 mg/kg
did not manifest any significant abnormal signs, behavioral changes, body weight changes, or

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macroscopic findings at any time of observation. There was no mortality in the above-mentioned
dose at the end of the 14 days of observation.
Effect of CECP on gastric ulcer induced by pylorus ligation
Gastric volume
A significant (P<0.01) increase in the gastric volume level is observed in the pylorus
ligated group when compared to the control group. CECP 200mg/kg and 400mg/kg treated group
have shown a significant (P<0.01) decrease in the gastric volume level and ranitidine treated
group have shown a significant (P<0.01) decrease in the gastric volume level when compared to
the Pylorus ligated group. The results were shown in Table 1.
pH
A significant (P<0.01) decrease in the pH level is observed in the pylorus ligated group
when compared to the control group. CECP 200mg/kg and 400mg/kg treated group have shown a
significant (P<0.05) and (P<0.01) increase in the pH level and ranitidine treated group have
shown a significant (P<0.01) increase in the pH level when compared to the Pylorus ligated
group. The results were shown in Table 1.
Ulcer number
A significant (P<0.01) increase in the ulcer number is observed in the pylorus ligated
group when compared to the control group. CECP 200mg/kg and 400mg/kg treated group have
shown a significant ( P,0.05) (P<0.01) decrease in the ulcer number and ranitidine treated group
have shown a significant (P<0.01) decrease in the ulcer number when compared to the Pylorus
ligated group. The results were shown in Table 1.
Ulcer severity score
A significant (P<0.01) increase in the ulcer severity score is observed in the pylorus
ligated group when compared to the control group. CECP 200mg/kg and 400mg/kg treated group
have shown a significant (P<0.01) decrease in the ulcer severity score and ranitidine treated
group have shown a significant (P<0.01) decrease in the ulcer severity score when compared to
the Pylorus ligated group. The results were shown in Table 1.
Free Acidity
A significant (P<0.01) increase in the free acidity is observed in the pylorus ligated group
when compared to the control group. CECP 200mg/kg and 400mg/kg treated group have shown a
significant (P<0.01) decrease in the free acidity and ranitidine treated group have shown a
significant (P<0.01) decrease in the free acidity when compared to the Pylorus ligated group. The
results were shown in Table 1.
Total acidity
A significant (P<0.01) increase in the total acidity is observed in the pylorus ligated group
when compared to the control group. CECP 200mg/kg and 400mg/kg treated group have shown a
significant (P<0.05) and (P<0.01) decrease in the total acidity and ranitidine treated group have
shown a significant (P<0.01) decrease in the total acidity when compared to the Pylorus ligated
group. The results were shown in Table 1.

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Total protein
A significant (P<0.01) increase in the total protein is observed in the pylorus ligated group
when compared to the control group. CECP 200mg/kg and 400mg/kg treated group have shown a
significant (P<0.05) and (P<0.01) decrease in the total protein and ranitidine treated group have
shown a significant (P<0.01) decrease in the total protein when compared to the Pylorus ligated
group. The results were shown in Table 1.
Effect of CECP on gastric ulcer induced by Ethanol
Ulcer index
A significant (P<0.01) increase in the ulcer index is observed in the ethanol induced group
when compared to the control group. CECP 200mg/kg and 400mg/kg treated group have shown a
significant (P<0.01) decrease in the ulcer index and ranitidine treated group have shown a
significant (P<0.01) decrease in the ulcer index when compared to the ethanol induced group. The
results were shown in Table 2.
Discussion
The antiulcer activity of CECP was studied in different models LIKE ulcers induced by
pylorus ligation and ethanol. Although the etiology of gastric ulcer is not known in most cases, it
is generally accepted that it results from an imbalance between aggressive factors and the
maintenance of mucosal integrity through the endogenous defense mechanisms [18].
It is well known that pylorus ligation causes gastric hypersecretion due to poorly
understood mechanisms. The activation of the vagus-vagal reflex by stimulation of pressure
receptors in the antral gastric mucosa in pylorus ligature model is believed to increase gastric
tonus and secretion [19]. Digestive effect of the accumulated gastric juice is belived to be
responsible for producing ulcers in the pylorus ligated rats. Pylorus ligated induced ulcers are
thought to be caused due to increased presence of acid and pepsin in the stomach. The essential
criteria, which determine the status of mucosal defense barrier against the offensive assault of
acid-pepsin is the quality and quantity of gastric mucus secretion. Increased mucus secretion by
the gastric mucosal cells can prevent gastric ulceration by several mechanisms including
lessening stomach wall friction during peristalsis and acting as an effective barrier to the back
diffusion of hydrogen ions [20].
The CECP reduces the gastric volume, ulcer score, free and total acidity of gastric acid
secretion of pylorus ligature induced gastric ulceration in rats. From results it is clear that the
CECP exhibited a significant gastric acid secretion activity by reducing the secretory parameters
when compared with the Pylorus ligated group. CECP pretreatment have shown a significant
reduction in protein levels when compared with group II. Hence, the protection by CECP against
gastric ulcers induced by Pylorus Ligated appears to be produced by the suppression of pepsin
levels and strengthening of mucosal barrier. Further, it is clear that the antiulcer activity against
this model was again found to be more with CECP extract.

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Table 1. Effect of CECP on acid secretary parameters in pylorus ligation induced gastric ulcer
Comparisons were made between: a- (Group I vs II), b- (Group II vs III, IV), C-(GroupII vs V)
Values are expressed as mean ± SEM of 6 animals. Statistical Significance test for comparison was done by ANOVA followed by Dunnet’s ‘t’ test.
Symbols represent statistical significance: ** P < 0.01, * P < 0.05, ns- non a significant.
Table 2. Effect of ulcer index in Ethanol induced gastric ulcer
Groups I
Control (CMC) II
Pylorus Ligated III
CECP 200mg/kg IV
CECP 400mg/kg V
Ranitidine 50mg/kg
Ulcer
index(mm2) 0.333±0.33 41.50 ±1.4a** 29.50 ± 0.92a** 18.67 ± 1.92b** 9.000 ± 1.0C**
Comparisons were between: a- (Group I vs II), b- (Group II vs III, IV), C-(GroupII vs V). Values are expressed as mean ± SEM of 6 animals. Statistical Significance test for
comparison was done by one way ANOVA followed by Dunnet’s ‘t’ test.
Symbols represent statistical significance: ** P < 0.01, * P < 0.05, ns- non a significant.
Groups
Gastric Volume
(ml/100g)
pH
Number of
Ulcer
Ulcer severity
score
Free acidity
(mEq/dl)
Total acidity
(mEq/dl)
Total protein
(µg/ml)
I
Control (CMC)
2.367 ± 0.15
2.91±0.15
0.1667±0.16
0.1667 ±0.1667
4.4480± 0.39
5.505 ± 0.0291
307.80 ± 8.01
II
Pylorus Ligated 7.033± 0.28a**
2.16 ±0.10a**
4.500±0.22a**
9.667± 0.61a**
7.617± 0.21 a**
8.358 ± 0.21a**
496.10 ± 6.45 a **
III
CECP 200mg/kg
6.333± 0.17b**
2.417 ± 0.15b*
3.500±0.34b*
7.333 ±0.55b**
6.598±0.11b**
7.928 ±0.35b*
385.64 ±5.89 b *
IV
CECP 400mg/kg
5.817 ± 0.11b**
3.00 ± 0.18b**
2.166±0.16b**
3.667± 0.61b**
4.405± 0.28b**
5.45 ± 0.20b**
325.26 ± 8.45 b **
V
Ranitidine50mg/kg
3.717 ± 0.13c**
3.583 ± 0.15c**
1.000±0.25c**
1.167± 0.30c**
3.058±0.11c**
4.038 ± 0.12c**
262.45 ± 6.76 b **

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Figure 1. Histopathology of pylorus ligated gastric ulcer stomach
I - Showing No Ulcer in Gastric Mucosa
II - Ulcer induced Gastric Mucosa showing ulcerated focus with detatching mucosal fragments
III - shows stomach mucosa at ulcer site superficial epithelium normal submucosa shows oedema
with congested vessels.
IV - Regenerating epithelium, compact glands .No sub mucosal oedema.
V - Hyperplastic Gastric Mucosa with no ulceration
Group I Group II
Grou
p
III Group IV
Group V

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Figure 2. Histopathology of ethnol induced gastric ulcer stomach
I - Showing No Ulcer in Gastric Mucosa
II - Ulcer induced Gastric Mucosa showing ulcerated focus with detatching mucosal fragments.
Submucosal oedema.
III - ulcer area showing regenerating epithelium. Submucosal oedema Present.
IV - The presence of regenerating epithelium. No congestion and inflammatory cells showing minimus
gastric mucosal ulcer.
V - Hyperplastic Gastric Mucosa with mimimus ulceration
Group I Group II
Group III Group IV
Group V

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Oral treatment with ethanol causes focal hyperemia, edema, necrosis and submucosal
hemorrhage as well as circulatory disturbances. The extent of ethanol-induced gastric mucosal
damage in rats correlates with the number of degranulating mast cells. Since these cells are a
source of several neuropeptides and inflammatory mediators, including histamine and
leukotrienes [21]. Ethanol induced gastric lesion formation may be due to stress in the gastric blood
flow which contributes to the development of hemorrhage and necrotic aspects of tissue injury.
Ethanol also increases Na+ and K+ flux into the lumen and increases pepsin secretion along with
the histamine release.HCL further deepens the necrosis and increases the tissue injury65. Ethanol
induced ulcer are more predominant in the glandular part of the stomach stimulates leukotrienes,
5-lioxygenase pathway, mast cell secretary product and breakdown of reactive oxygen species
resulting in the damage of gastric mucosa.Another action promoted by ethanol is its ability to
damage the gastric mucosa by mechanical injury [22].
The results further indicate that CECP may enhance gastric mucosal defensive factor, such
as mucus and or prostaglandin. Therefore protection afforded by CECP against ethanol induced
gastric ulceration could also be due to inhibition of the 5-lipoxygenase pathway or to the
antagonistic activity of leukotrienes. Flavonoids are capable of protecting the gastric mucosa from
necrotizing substances and possible useful in the therapy of acute and chronic gastric ulcerations.
plant-originated flavanoid substances such as Solon- Sophoradin root, seed extract of
Amaranth, extract of grapefruit seeds - Citro, and capsaicin present in chilli pepper extract are
beneficial and dose-dependent reduction in acute and chronic gastric lesions. Plant-originated
flavonoid substances are highly gastroprotective [23].
The Antiulcer effect of the lipid components of M. azedarach fruits which is mainly due to
the phytosterol fraction [24,25].Sterols may even protect against peptic ulcer diseases even in the
area of prevalence of H.pylori. Phytosterol esters and sterols, in horse gram an herb in the genus
Dolichos cultivated in India for food and fodder were protective for ulcers [26].
Phytochemical studies of the chloroform extract of Cayratia pedata Lam revealed the
presence of flavonoids, sterols and terpenes. Numerous flavonoids have shown reducing gastric
acid secretion and protective properties in different experimental model. Phytosterols which
have been shown various properties that is necessary for protection against ulcer induction. Since
flavonoids and sterols shown to be present in the, chloroform extract of Cayratia pedata Lam
these constituents may be responsible for the anti-ulcer activity of the chloroform extract of
Cayratia pedata Lam.
Therefore, it can be concluded that this crude extract have a potential to be used as an
antiulcer drug in combination with other drugs or alone. Though the mechanism of the Anti-ulcer
action of the plant extract remains to be studied in detail. Isolation of the active constituents may
be carried in future.
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