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Toxicological information

Repeated dose toxicity: other routes

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Administrative data

Endpoint:
sub-chronic toxicity: other route
Type of information:
migrated information: read-across from supporting substance (structural analogue or surrogate)
Adequacy of study:
weight of evidence
Reliability:
3 (not reliable)
Rationale for reliability incl. deficiencies:
other: Unsuitable test system (One dose or multiple doses with cafeic acid tested via I.P. injection).
Cross-referenceopen allclose all
Reason / purpose:
reference to same study
Reason / purpose:
reference to other study

Data source

Reference
Reference Type:
publication
Title:
Efficacy of caffeic acid in preventing nickel induced oxidative damage in liver of rats
Author:
Pari, L. and A. Prasath.
Year:
2008
Bibliographic source:
Chemico-Biological Interactions. 173:77–83

Materials and methods

Test guideline
Guideline:
other: Not reported
GLP compliance:
yes
Limit test:
no

Test material

Reference
Name:
Unnamed
Type:
Constituent
Type:
Constituent
Type:
Constituent

Test animals

Species:
rat
Strain:
Wistar
Sex:
male
Details on test animals and environmental conditions:
Adult male albino rats of Wistar strain (150–170 g)were used for the experiment. The animals were housed in plastic
cages and maintained in 12-h light/12-h dark cycle, 50% humidity and 25±3 ◦C. The animals had free access to
standard pellet diet (M/S. Pranav Agro Industries Ltd., Bangalore, India) and water ad libitum.

Administration / exposure

Route of administration:
intraperitoneal
Vehicle:
other: Isotonic saline
Details on exposure:
Group 1: control rats treated intraperitoneally with isotonic saline for 20 days.
Group 2: control rats received Caffeic Acid (CA) (60 mg/kg body weight) in aqueous solution daily using intragastric tube for 20 days.
Group 3: rats received Ni as nickel sulfate (20 mg/kg body weight) intraperitoneally in isotonic saline for 20 days.
Group 4–6: rats received Ni intraperitoneally (20 mg/kg/body weight) with oral administration of CA (15, 30 and 60 mg/kg/body weight) in
aqueous solution for 20 days.
Duration of treatment / exposure:
20 days
Frequency of treatment:
Daily
Doses / concentrations
Remarks:
Doses / Concentrations:
20 mg/kg body weight
No. of animals per sex per dose:
6
Control animals:
yes, concurrent vehicle

Examinations

Statistics:
Data were analysed by one way analysis of variance (ANOVA) followed by Duncan’s multiple range test (DMRT)
Results were presented as mean±S.D. p-Values < 0.05 were considered as statistically significant.

Results and discussion

Results of examinations

Details on results:
Ni induced liver damage was clearly shown by the increased activities of serum hepatic enzymes namely aspartate transaminase (AST), alanine
transaminase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT) and lactate dehydrogenase (LDH) along with increased elevation of lipid peroxidation indices (thiobarbituric reactive acid substances (TBARS) and lipid hydroperoxides).

The toxic effect of Ni was also indicated by significantly decreased levels of enzymatic (superoxide dismutase (SOD), catalase (CAT)
glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (glutathione (GSH), vitamin C and vitamin E).

Target system / organ toxicity

Critical effects observed:
not specified

Applicant's summary and conclusion

Executive summary:

STUDY RATED BY AN INDEPENDENT REVIEWER.