ArticlePDF Available

Toxicity Effects of Hair Dye Application on Liver Function in Experimental Animals

Authors:

Abstract and Figures

Abstract Objective: This study was conducted to assess the hair dye toxicity by using hair dye among experimental rats in order to verify the biochemical and haematological abnormalities and liver dysfunction. Methods: Albino Wistar Rats were obtained from the Faculty of Pharmacy, University of Khartoum– Sudan. The rats were divided into two batches on the basis of using the commercial hair dye as oral or subcutaneous administration respectively; each batch has four groups (control and three test groups) each comprising six rats. Batch-1 (group-2, 3, and 4 orally administered with 10, 20, and 30mg/kg body weight of the commercial hair dye, respectively); and Batch-2 (group-2, 3, and 4 subcutaneously administered with 10, 20, and 30 mg/kg body weight of the commercial hair dye, respectively). Results: The clinical features were shown in all rats batches, administered orally or subcutaneously with the commercial hair dye. These clinical features rates from slight weakness in group 2 to head, neck, and pharyngeal oedema in group-3 up to severe weakness in hinds and fore limbs with election of hair, tremors, shivering of the whole body and respiratory distress, severe convulsions, and respiratory difficulty prior to death in group-4. The Biochemical parameters showed significant (P<0.05) increase in the activities of the liver enzymes concomitant with the increase of the commercial hair dye dosage in the two batches, and decrease in the total plasma protein levels, albumin, and cholesterol with the increase of commercial hair dye dosage in the two batches. Hematological parameters showed a significant (p value <0.05) decrease in complete blood count (associated with significant decreases in neutrophils and significant increases of lymphocytes) concomitant with the increasing of commercial hair dye concentration. Conclusion: The study highlighted the major toxicity of commercial hair dye and its association with liver function
Content may be subject to copyright.
Toxicity Effects of Hair Dye Application on Liver Function in Experimental
Animals
Ehab Ibrahim Salih El-Amin1*, Mohammed Abd AL Rahim GahElnabi2, Waled Amen Mohammed Ahmed3, Ragaa Gasim Ahmed4 and Khalid Eltahir Khalid5
1Assistant Professor of Human Anatomy, Albaha University, Faculty of Applied Medical Sciences, Head of Community Health Department, Kingdom of Saudi Arabia
2Professor of Forensic Medicine and Toxicology, National Ribat University, College of Sudanese Police Sciences, Sudan
3Assistant Professor of Nursing, Albaha University, Faculty of Applied Medical Sciences, Nursing Department, Kingdom of Saudi Arabia
4Assistant Professor of Nursing, Albaha University, Faculty of Applied Medical Sciences, Nursing Department, Kingdom of Saudi Arabia
5Associate Professor of Biochemistry, Albaha University, Faculty of Applied Medical Sciences, Department of Medical Laboratory Sciences, Kingdom of Saudi Arabia
*Corresponding author: Dr. Ehab Ibrahim Salih El-Amin, PhD, Albaha University, Faculty of Applied Medical Sciences, Head of Community Health Department,
Kingdom of Saudi Arabia, Tel: 00966502576218; Email: ehabsalih2000@yahoo.com
Received date: Jun 19, 2014, Accepted date: Aug 27, 2014, Published date: Aug 29, 2014
Copyright: © 2014 Salih El-Amin EI, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Objective: This study was conducted to assess the hair dye toxicity by using hair dye among experimental rats in
order to verify the biochemical and haematological abnormalities and liver dysfunction.
Methods: Albino Wistar Rats were obtained from the Faculty of Pharmacy, University of Khartoum– Sudan. The
rats were divided into two batches on the basis of using the commercial hair dye as oral or subcutaneous
administration respectively; each batch has four groups (control and three test groups) each comprising six rats.
Batch-1 (group-2, 3, and 4 orally administered with 10, 20, and 30mg/kg body weight of the commercial hair dye,
respectively); and Batch-2 (group-2, 3, and 4 subcutaneously administered with 10, 20, and 30 mg/kg body weight of
the commercial hair dye, respectively).
Results: The clinical features were shown in all rats batches, administered orally or subcutaneously with the
commercial hair dye. These clinical features rates from slight weakness in group 2 to head, neck, and pharyngeal
oedema in group-3 up to severe weakness in hinds and fore limbs with election of hair, tremors, shivering of the
whole body and respiratory distress, severe convulsions, and respiratory difficulty prior to death in group-4. The
Biochemical parameters showed significant (P<0.05) increase in the activities of the liver enzymes concomitant with
the increase of the commercial hair dye dosage in the two batches, and decrease in the total plasma protein levels,
albumin, and cholesterol with the increase of commercial hair dye dosage in the two batches. Hematological
parameters showed a significant (p value <0.05) decrease in complete blood count (associated with significant
decreases in neutrophils and significant increases of lymphocytes) concomitant with the increasing of commercial
hair dye concentration.
Conclusion: The study highlighted the major toxicity of commercial hair dye and its association with liver
dysfunction.
Keywords: Hair dye; Paraphenylenediamine; Toxicity; Liver
atrophy; Parameters; Experimental animals; Sudan
Introduction
Henna is very popular culture in Sudan; it is part of the traditions
which used to adorn women’s body during marriage ceremonies and
other social celebrations since the Bronze Age. Henna is commercially
cultivated in Sudan and other countries. Despite the wide spread use of
natural henna, reports of allergic contact dermatitis to natural henna
are very rare in the literature. It can therefore be assumed that natural
henna is safe [1]. The first artificial dye was synthesized in the
laboratory in 1856, and permanent hair colorants have been in
commercial use for over 100 years [2].
Para-Phenylenediamine (PPD) is an organic compound; its
chemical formula is C6H8N2 [3]. This derivative of aniline is a white
solid, but samples can darken due to air oxidation. It is also an
ingredient used in Sudan and other countries in combination with
henna “lawasonia Alba” for tattooing to give black color in a short
time in traditional and during local and social festival. It was found to
be toxic and there are some reports from these countries showing its
toxicity on different systems of the body. The consumers use this
product because its price is 20-30 times less expensive than
pharmaceutical hair dye preparations [4].
Many accidental cases of toxicity and mortality have been reported
in Sudan, Egypt and other countries in cases of suicidal and homicidal
due to oral ingestion or subcutaneous mistaken used of hair dyes
containing Para-phenylenediamine [5]. There are many studies
showed effects on respiratory, renal, and muscular system, but no
study determines the effects on all these systems together, and no
study describes the correlation of PPD toxicity to body's biochemical
alterations in liver [6].
Clinical Toxicology Salih El-Amin et al., J Clin Toxicol 2014, 4:4
http://dx.doi.org/10.4172/2161-0495.1000210
Research Article Open Access
J Clin Toxicol
ISSN:2161-0495 JCT, an open access journal Volume 4 • Issue 4 • 1000210
There was a continuous inflow of suicidal and homicidal cases in
Sudanese hospitals and the causes of poisoning with PPD are much
conflicting in the determination of clinical order of PPD Patients [7].
As PPD is the main ingredient on hair dyes, and whose toxicity is
directly related to human health. So this paper studied the toxicity of
hair dye in vivo, to determine the biochemical and haematological
abnormalities associated with major toxicity of commercial hair dye
and liver dysfunction among experimental animals.
Methodology
This study was conducted at national research center-University of
Khartoum. The commercial hair dye was collected from local markets
(Libya Market–Omdurman).
Albino Wistar male rats at age of 11 weeks, weighting 140-160 g
were obtained from the Faculty of Pharmacy, University of
Khartoum–Sudan. The animals were housed in cages provided with
rice husk as bedding materials and kept under ambient temperature of
23 ± 2°C. The animals were kept in the laboratory condition for 1 week
to adapt the climate condition and for the commencement of
treatment protocol. The rats were divided into two batches on the
basis of using the commercial hair dye as oral or subcutaneous
administration respectively; each batch has four groups (control and
three test groups) each comprising six rats. Batch-1 (group-2, 3, and 4
orally administered with 10, 20, and 30 mg/kg body weight of
commercial hair dye, respectively); and Batch-2 (group-2, 3, and 4
subcutaneously administered with 10, 20, and 30 mg/kg body weight
of commercial hair dye, respectively). The animals were killed after 3-6
days after the administration. The lethal dose of commercial hair dye
for rats was determined as 80 mg/kg body weight [8] and the lethal
subcutaneous dose was determined as 37 mg/kg body weight [9].
Hence, we tested the toxicity of various sub lethal doses through
different routes considering the LD50 of PPD is 37 mg/kg.
Two milliliter of blood samples were collected from eye blood
vessels of each rat in ethylenediamine tetra acetic acid (EDTA)
container for hematological tests and other 2 ml of blood samples were
collected in heparinized containers for biochemical tests. Plasma was
separated by centrifugation at 3000 rpm for 5 min.
Total proteins, glucose, cholesterol, albumin, and the enzyme
activities of GOT, GPT, and ALP were measured
spectrophotometrically by using commercial kits. Determination of
hemoglobin concentration (Hb), packed cell volume (PCV), red blood
cells (RBCs) count, and total white blood cell (TWBC) count, mean
corpuscular volume (MCV), mean corpuscular hemoglobin
concentration (MCHC) and mean corpuscular hemoglobin (MCH),
PLT count, (Lymphocytes–Basophil, Neutrophil) were analyzed by a
semi-automated hematological analyzer (Sysmex Corporation;
Mundelein, Illinois, Sysmex America, Inc.).
Statistical analyses were performed using statistical package for
social sciences (SPSS) version 11.5 and excel 2007 statistical program.
Continuous and categorical variables were analyzed using student’s t-
test and Chi-square test respectively. P value was considered
significant if it was less than 0.05.
Results
Clinical features were shown in all rats administered orally or
subcutaneously with the commercial hair dye, however, the clinical
features rate from slight weakness in group 2 to head, neck, and
pharyngeal oedema in group-3 up to severe weakness in hinds and
fore limbs with election of hair, tremors, shivering of the whole body
and respiratory distress, and there were severe convulsions and
respiratory difficulty prior to death which occurred at about four
hours post oral ingestion of the commercial hair dye in group-4. As
seen in Table 1 and Table 2, the biochemical parameters showed
significant (P<0.05) increase in activities of the liver enzymes
glutamate oxalotranserase (GOT), glutamate pyruvate transferase
(GPT), and alkaline phosphatase (ALP), and there is a decrease in the
total plasma protein levels, albumin, and cholesterol when compared
with the control groups.
Groups /
Parameters
Group 1
(Control)
Group 2 (10
mg/kg)
Group 3 (20
mg/kg) Group 4 (30
mg/kg)
GOT (U/L) 41.3 ± 2.1 1219.5 ±
12.1***
1581.8 ±
30.9***
1690.0 ±
23.7***
GPT (U/L) 40.1 ± 1.7 127.8 ±
1.2*** 242.8 ± 7.2*** 295.0 ±
28.8***
ALP (U/L) 115.3 ± 3.2 113.7 ± 2.8 129.0 ± 1.4* 136.0 ± 2.2**
T. proteins
(g/dl) 7.5 ± 0.7 7.0 ± 0.6 6.7 ± 0.3 6.3 ± 0.5*
Glucose
(mg/dl) 105.3 ± 11.0 137.8 ± 1.7** 127.8 ± 0.8* 113.5 ± 3.6
Cholesterol
(mg/dl) 88.5 ± 15.8 60.2 ± 5.9*** 67.5 ± 4.4** 79.0 ± 3.7*
Albumin (g/dl) 4.2 ± 0.7 4.8 ± 0.3 3.7 ± 0.3* 3.2 ± 0.2*
* = P<0.05; ** = P<0.01; *** = P<0.001
Table 1: Showing the mean differences of Biochemical parameters
between the study groups when received different oral ingestion doses
(10-20-30 mg/kg b.w.) using the commercial hair dye.
Groups / Parameters Group 1
(Control)
Group 2 (10
mg/kg)
Group 3 (20
mg/kg)
Group 4
(30 mg/kg)
GOT (U/L) 41.3 ± 2.1 1311.7 ±
3.1***
1663.7 ±
2.3***
1790.5 ±
1.0***
GPT (U/L) 40.1 ± 1.7 138.0 ±
0.9***
242.3 ±
2.2***
302.0 ±
2.1***
ALP (U/L) 115.3 ± 3.2 112.2 ± 1.9 129.0 ±
1.4*
136.7 ±
2.1**
T. proteins (g/dl) 7.5 ± 0.7 6.8 ± 0.4 6.5 ± 0.3 6.0 ± 0.2*
Glucose (mg/dl) 105.3 ± 11.0 138.8 ± 2.1** 127.3 ±
2.2*
115.3 ± 2.2
Cholesterol (mg/dl) 88.5 ± 15.8 59.5 ± 1.9*** 65.8 ± 1.5** 77.2 ± 3.0*
Albumin (g/dl) 4.2 ± 0.7 4.8 ± 0.3 3.7 ± 0.1* 3.9 ± 0.3
* = P<0.05; ** = P<0.01; *** = P<0.001
Table 2: Showing the mean differences of Biochemical parameters
between the study groups when received different subcutaneous doses
(10-20-30 mg/kg b.w.) using the commercial hair dye.
These differences associated with the increase of the commercial
hair dye dosage in the two batches. Blood glucose showed significant
Citation: Salih El-Amin E, AL Rahim GahElnabi MA, Mohammed Ahmed WA, Gasim Ahmed R, Eltahir Khalid K (2014) Toxicity Effects of Hair
Dye Application on Liver Function in Experimental Animals. J Clin Toxicol 4: 210. doi:10.4172/2161-0495.1000210
Page 2 of 5
J Clin Toxicol
ISSN:2161-0495 JCT, an open access journal Volume 4 • Issue 4 • 1000210
increase among different doses of oral or subcutaneous commercial
hair dye compared with the control groups. Despite the different route
of commercial hair dye administration, the results showed slight
increase in the mean results of GOT, GPT and total protein when the
commercial hair dye administered subcutaneously.
Compared with the control groups, hematological parameters
showed significant (p value <0.05) decrease in Hb, RBCs, PCV,
TWBCs count (associated with significant decreases in neutrophils
and significant increases of lymphocytes), MCH, and MCV relevant to
the increasing of the commercial hair dye concentration. Despite the
significant decreases (P<0.05) in the percentage of neutrophils count,
the platelets and lymphocytes showed significant (P<0.05) increase
associated with increasing concentrations of the commercial hair dye
in the different routes (Table 3 and Table 4).
Groups / Parameter Group 1 (Control) Group 2 (10 mg/kg) Group 3 (20 mg/kg) Group 4 (30 mg/kg)
12.85 ± 0.67 10.38 ± 0.73* 9.59 ± 0.68* 8.67 ± 0.82**
44.67 ± 0.52 37.57 ± 0.88* 27.00 ± 2.83*** 25.33 ± 2.73***
35466.00 ± 859.45 5116.67 ± 231.66* 4083.33 ± 365.60** 3483.33 ± 172.24***
7600.00 ± 2182.65 5133.33 ± 2182.66*** 4133.33 ± 659.29*** 2900.00 ± 209.76***
29.83 ± 2.32 20.0 ± 2.19* 18.33 ± 1.97** 16.67 ± 2.07***
88.67 ± 5.32 65.00 ± 4.15*** 59.67 ± 7.61*** 52.17 ± 4.83***
34.00 ± 1.41 37.50 ± 2.74 42.83 ± 3.71* 45.50 ± 2.51**
240833.3 ± 82366.1 203333.3 ± 25819.9** 373333.3 ± 25819.9*** 558333.3 ± 34302.6***
27.83 ± 6.18 54.33 ± 3.61*** 67.50 ± 5.13*** 87.33 ± 3.27***
0.52 ± 0.37 0.57 ± 0.34 0.72 ± 0.21*** 0.87 ± 0.61***
54.50 ± 9.29 24.67 ± 2.16*** 10.35 ± 1.65*** 6.67 ± 1.63***
*=P<0.05; **=P<0.01; ***=P<0.001
Table 3: Showing the mean differences of Hematological parameters between the study groups when received different oral doses (10-20-30
mg/kg b.w.) using the commercial hair dye.
Groups / Parameters Group 1 (Control) Group 2 (10 mg/kg) Group 3 (20 mg/kg) Group 4 (30 mg/kg)
Hb (g/dl) 12.85 ± 0.67 10.23 ± 0.64* 9.32 ± 0.5* 8.67 ± 0.82**
PCV (%) 44.67 ± 0.52 29.87 ± 2.25*** 27.83 ± 2.14*** 25.50 ± 1.87***
RBCs˟103/CMM 5466.00 ± 859.45 5400.00 ± 740.27 3883.33 ± 147.20** 3700.00 ± 442.72***
TWBCs /CMM 7600.00 ± 2182.65 4983.33 ± 231.66*** 3366.67 ± 463.32*** 2816.67 ± 318.85***
MCH (pg) 29.83 ± 2.32 20.98 ± 2.04* 19.17 ± 1.94* 15.33 ± 1.37***
MCV (fl) 88.67 ± 5.32 65.17 ± 1.94*** 65.67 ± 3.31*** 57.17 ± 3.31***
MCHC (g/dl) 34.00 ± 1.41 34.17 ± 2.14 36.83 ± 2.93 46.50 ± 2.43**
PLT /CMM 240833.3 ± 82366.1 277666.7 ± 29024.5** 358333.3 ± 29268.9*** 555000.0 ± 32710.9***
LYM% 27.83 ± 6.18 55.50 ± 2.43*** 76.83 ± 2.86*** 88.33 ± 4.27***
BASO% 0.52 ± 0.37 0.38 ± 0.17*** 0.53 ± 0.27 0.73 ± 0.22***
NEUT% 54.50 ± 9.29 20.67 ± 2.88*** 10.17 ± 1.17*** 6.83 ± 1.47***
*= P<0.05; **= P<0.01; ***= P<0.001
Table 4: Showing the mean differences of Hematological parameters between the study groups whenreceived different subcutaneous doses
(10-20-30 mg/kg b.w.) using the commercial hair dye.
Citation: Salih El-Amin E, AL Rahim GahElnabi MA, Mohammed Ahmed WA, Gasim Ahmed R, Eltahir Khalid K (2014) Toxicity Effects of Hair
Dye Application on Liver Function in Experimental Animals. J Clin Toxicol 4: 210. doi:10.4172/2161-0495.1000210
Page 3 of 5
J Clin Toxicol
ISSN:2161-0495 JCT, an open access journal Volume 4 • Issue 4 • 1000210
Discussion
This study was carried out to evaluate the hair dye toxicity by using
commercial hair dye in a way to estimate the hazards of this dye on
rats, since it is known that toxic effects in humans are usually in the
same range as those of experimental animals. PPD is the main
constituent in hair dye and is an organic derivative of paranitroaniline,
when ingested in a dose-dependent manner, results in severe
hypersensitivity (itching, angioedema, asphyxia) and rhabdomyolysis
(paresis of extremities, cola-colored urine, oliguria, markedly elevated
creatinine phosphokinase and lactate dehydrogenase, hyperkalemia,
hypophosphatemia and hypocalcaemia) [10,11]. Other features such as
anemia, leukocytosis, hemoglobinemia, hemoglobinurea, and liver
necrosis have been reported [12]. In animal model, PPD induces
rhabdomyolysis leakage of calcium ions from the smooth endoplasmic
reticulum, followed by continuous contraction and irreversible
structural changes in the muscles [13].
In this study, we used commercial hair dye given to Albino Wistar
rats in order to provide information about the effect of commercial
hair dye on liver as hepatocellular necrosis accompanying hair dye
poisoning in human [12].
The commercial hair dye was introduced in this study through oral
and subcutaneous routes, although the variation in systemic effect
between the two routes was not great. As shown in the results,
subcutaneous injection results in a rather faster absorption of
commercial hair dye than oral ingestion but the difference are not
great.
At higher doses of the commercial hair dye, there was broad
deviation from the normal values in biochemical and hematological
parameters compared to lower doses of hair dye administered via the
same route in all batches, because the concentration of a toxic agent
influence its rate of absorption.
Our results showed significant increase in liver enzymes (GOT,
GPT, ALP) activities in a dose-dependent manner in the two batches,
and there is a decrease in the total plasma protein levels, albumin, and
cholesterol associated with the increase of the commercial hair dye
dosage in the two batches. Our finding is in agreement with others
[14-18] when their administration of PPD to rats revealed a significant
increase in GOT, GPT, and ALP, and a significant decrease in total
proteins and glucose. Blood glucose showed significant increase
among different doses of oral and subcutaneous administration of
commercial hair dye compared with the control groups. Our result
showed inconsistency with other study reported that the PPD leads to
renal failure resulting in appreciable amount of urine glucose which
causes low blood glucose level in rats [17]. Changes in the
aforementioned biochemical parameters in our study indicate possible
hepatic toxicity, pointed out by the substantial leakage of enzymes
contained in the cells of hepatic tissues to the blood. It has been
reported that low cholesterol level is usually associated with
hepatocellular damage [18-19]. The decrease in the level of cholesterol
in our study may be associated with hepatic lipidosis and obstructive
liver diseases [20].
The hematological investigations showed significant decrease in Hb
and PCV values which may be attributed to the escape of plasma from
circulation to the surrounding tissues, in addition to significant
decreases in RBCs, MCH and MCV values. These hematological
changes indicate that, anemia may occur as a result of exposure to
commercial hair dye. The possible cause for anemia is the hemolytic
effect of PPD on RBCs; anemia was noticed in rats that received sub
lethal doses of PPD, however, in chronic toxicity experiments, all
batches showed hematological changes indicating anemia. The effect
of commercial hair dye on RBCs may extend to bone marrow leading
to inadequate production of red blood cells and other elements. The
decrease in MCH and MCV has been associated with macrocytic
anemia, while the decrease in MCHC values indicates anemia and iron
deficiency.
In this study, TWBC count was found to be decreased in rats that
received different doses of commercial hair dye and have been
associated with significant decrease in neutrophil cells and significant
increase in lymphocyte cells. This may be due to the action of PPD in
the immune system, which triggers neutrophils apoptosis and massive
production of immunocompetent cells [21].
The changes in biochemical and hematological parameters were
reported more significantly among rats exposed to higher doses of
commercial hair dye.
Our study highlighted the experimental correlation between
commercial hair dye administration and liver dysfunction, and reflects
the importance of public awareness regarding the potential lethality of
commercial hair dye and the governmental legislations and restriction
of sale of commercial hair dye.
Authors' Contribution
The main investigator of this work is Dr. Ehab Salih and all other
authors contributed equally in this work.
References
1. Pasricha JS, Gupta R, Panjwani S (1980) Contact dermatitis to henna
(Lawsonia). Contact Dermatitis 6: 288-289.
2. http/www.ScienceLab.com
3. Scientific Committee on Consumer Products (SCCP) Opinion on P-
phenylenediamine. Public Health and Risk Assessment; 9th plenary
meeting; Brussels, Belgium.
4. European Commission Health and Consumer Protection Directorate-
General. Opinion on p-Phenylenediamine. Scientific Committee on
Consumer Products. SCCP/0989/06.
5. Ahmed HA, Abdel Maaboud RM, Abdul Latif FF, Kamal El-Dean AM,
El-Shaieb KM (2013) Different Analytical Methods of Para-
Phenylenediamine Based Hair Dye. Journal of Cosmetics, Dermatological
Sciences and Applications. 3: 17-25
6. El-Ansary EH, Ahmed ME, Clague HW (1983) Systemic toxicity of para-
phenylenediamine. Lancet 1: 1341.
7. Sood AK, Yadav SP, Sood S, Malhotra RC (1996) Hair dye poisoning. J
Assoc Physicians India 44: 69.
8. European Commission Health and Consumer Protection Directorate-
General. Opinion on p-Phenylenediamine. Scientific Committee on
Consumer Products. SCCP/0989/06.
9. Http/www.ScienceLab.com
10. Sandeep Reddy Y, Abbdul Nabi S, Apparao C, Srilatha C, Manjusha Y, et
al. (2012) Hair dye related acute kidney injury--a clinical and
experimental study. Ren Fail 34: 880-884.
11. Soni SS, Nagarik AP, Dinaker M, Adikey GK, Raman A (2009) Systemic
toxicity of paraphenylenediamine. Indian J Med Sci 63: 164-166.
12. Singla S, Miglani S, Lal AK, Gupta P, Agarwal AK (2005) Para-
phenylenediamine (PPD) poisoning. Journal, Indian Academy of Clinical
Medicine 6:136-138.
13. Curtis DK, Mary OA, John Doull (1986). Casarett and Doulls
Toxicology- The basic Science of Poisons, Macmillan Publishing
Company. New York.
Citation: Salih El-Amin E, AL Rahim GahElnabi MA, Mohammed Ahmed WA, Gasim Ahmed R, Eltahir Khalid K (2014) Toxicity Effects of Hair
Dye Application on Liver Function in Experimental Animals. J Clin Toxicol 4: 210. doi:10.4172/2161-0495.1000210
Page 4 of 5
J Clin Toxicol
ISSN:2161-0495 JCT, an open access journal Volume 4 • Issue 4 • 1000210
14. Spector WS (1955) Hand book of Toxicology. Vol. 1. Acute toxicities of
solids, liquids and gases to laboratory animals. Philadelphia, PA: W. B.
Saunders Co., pp-232.
15. Saito K, Murai T, Yabe K, Hara M, Watanabe H, et al. (1990)
[Rhabdomyolysis due to paraphenylenediamine (hair dye)--report of an
autopsy case]. Nihon Hoigaku Zasshi 44: 469-474.
16. Averbukh Z, Modai D, Leonov Y, Weissgarten J, Lewinsohn G, et al.
(1989) Rhabdomyolysis and acute renal failure induced by
paraphenylenediamine. Hum Toxicol 8: 345-348.
17. Bourquia A, Jabrane AJ, Ramdani B, Zaid D (1988) [Systemic toxicity of
paraphenylenediamine. 4 cases. Presse Med 17: 1798-1800.
18. Hyde TA Chemistry In Raphael SS (1983) Lynchs Medical Laboratory
Technology (4th edn) WB Saunders Company.
19. MIZRAHI IJ, EMMELOT P (1962) The effect of cysteine on the
metabolic changes produced by two carcinogenic Nnitrosodialklamines
in rat liver. Cancer Res 22: 339-351.
20. Jack HD, Michael JM, Edward CW (1986) Toxic response of immune
system. In Curtis DK, Mary OA, John Doul MD (Eds) Casarett and
Doulls Toxicology the Basic Science of poison. Macmillan publishing Co,
pp-245-251.
21. Elyoussoufi Z, Habti N, Mounaji K, Motaouakkil S, Cadi R (2013)
Induction of oxidative stress and apoptosis in human neutrophils by p-
phenylenediamine. Journal of Toxicology and Environmental Health
Sciences 5: 142-149.
Citation: Salih El-Amin E, AL Rahim GahElnabi MA, Mohammed Ahmed WA, Gasim Ahmed R, Eltahir Khalid K (2014) Toxicity Effects of Hair
Dye Application on Liver Function in Experimental Animals. J Clin Toxicol 4: 210. doi:10.4172/2161-0495.1000210
Page 5 of 5
J Clin Toxicol
ISSN:2161-0495 JCT, an open access journal Volume 4 • Issue 4 • 1000210
... This increase of liver enzymes may be attributed to the hepatocellular damage resulting from chemical toxicity, where these enzymes levels showed an intimate relationship to cell necrosis and/or increased cell membrane permeability that leads to discharge of the enzyme to blood stream and increase of its level in serum [13]. Our results are coincident with the study of Salih et al., (2014) [14] who detected a significant increase in liver enzymes (GOT and GPT) activities in a dose-dependent manner after oral or subcutaneous administration of hair dye (PPD is the main constituent in hair dye and is a derivative of paranitroaniline). While, the marked decrease in total protein level was markedly decreased in treated rats with low and high doses of Sudan III may attributed to the cellular damage caused by Sudan III metabolites or due to oxidative stress [15]. ...
... Serum levels of cholesterol, Trig and LDL were considerably increased in rats received high and low doses of Sudan III. In contrary to the present findings, Salih et al., (2014) [14] reported that low cholesterol level observed in his study is usually associated with hepatocellular damage, hepatic lipidosis and obstructive liver diseases [17]. ...
Article
Full-text available
Azo compounds were widely used in industry. Although they are not permitted in food, they had been found contaminating different foodstuffs. In the present study, the geno and hepatotoxic effects of Sudan III were estimated with relation to oxidative stress. Rats (n=18) were randomly divided into three groups each of 6. First group were left as control, the remaining two groups, were orally administrated either 125 mg/kg body weight of Sudan III (1/40 LD 50), or 250 mg/kg body weight of Sudan III (1/20 LD 50) for consecutive 45 days. Rats then sacrificed, blood and tissue samples were harvested. DNA was extracted then fragments were analyzed in the automatic multicapillary electrophoresis, the serum activity of GOT and GPT were measured. Moreover, serum Glu, Alb and TP were evaluated. Lipid profiles were assessed through measuring of Chol, Trig, HDL and LDL. Liver GSH, CAT, SOD and MDA concentrations were evaluated. Our results revealed that, oral administration of Sudan III for 45 days caused serum Glu, GOT and GPT activities to increase significantly (P<0.05) in low and high doses. The TP level was markedly decreased (P<0.05) in treated rats with low and high doses of Sudan III, while there was no significant differences in Alb for both doses between groups. Serum level of Chol, Trig, and LDL were significantly increased (P<0.05) in rats received low and high doses of Sudan III compared to that in control untreated rats, while HDL showed significant decreased (P<0.05) in both doses of Sudan III compared to that in control untreated rats. GSH, SOD and CAT were significantly (P<0.05) decreased in liver tissues of rats received low and high doses of Sudan III compared to that in control untreated rats, While MDA level was increased significantly (P<0.05) in liver tissue of rats received high Sudan III dose, beside oxidative DNA damage with appearance of new bands in both low and high doses of Sudan III. In conclusion, low and high doses of Sudan III dye triggered the hepatocellular damage and adversely altered the lipid and oxidative stress biomarkers in male rats after 45 days of oral administration with induction of genotoxicity.
Article
Introduction: Paraphenylenediamine is the main component in many commercial hair dyes, and can produce severe local and systemic toxicity reactions after acute ingestion or dermal absorption. The aim of this study was to assess the factors contributing to morbidity and mortality in cases of acute paraphenylenediamine poisoning, with a focus on evaluating the resultant hepatic and cardiac toxicity. Methods: This observational study was conducted on patients with acute paraphenylenediamine poisoning presenting to Sohag University Hospitals, and included a retrospective part from February 2021 to January 2022 and a prospective part from February 2022 to July 2022. Clinical data were extracted and receiver operating characteristic curves created to identify prognostic markers. Results: Among 50 eligible patients 39 (78 percent) recovered, and 11 (22 percent) died or had permanent complications. Angioedema and anuria were the most frequent features in complicated cases. By receiver operating characteristic analysis, either an increase in aspartate aminotransferase activity greater than 644 IU/L or alanine aminotransferase activity greater than 798 IU/L, a time delay to presentation of greater than 4.5 hours, and a pH of less than 7.32 were associated with a significant increase in morbidity and mortality. While cardiac enzyme activities, and concentrations of blood urea nitrogen and creatinine increased in most cases, they were not associated with mortality. Discussion: Management of patients with paraphenylenediamine poisoning is mainly supportive, as there is no specific antidote. Respiratory failure and kidney failure are the most life threatening complications. Hepatoxicity and cardiotoxicity also occur. The ability to predict the events can help guide patient disposition and care. Conclusion: Elevated liver enzyme activities, increased time delay to admission, decreased pH, and the presence of angioedema and anuria can be used as predictors of morbidity and mortality in patients with acute paraphenylenediamine poisoning.
Article
Full-text available
Many cases of toxicity and mortality either due to accidental or deliberate ingestion of hair dyes were reported in Egypt, Sudan, Israel, Morocco, Saudi Arabia, India and Tunisia. In the field of forensic analytical toxicology, the identification and quantification of chemicals are essential in deaths related to intoxication. The aim of the present study is to conduct chemico-analytical characterization of para-phenylenediamine (PPD) based hair dye of (Black stone hair dye, SHD) currently used for dying hear in Egypt, to confirm the identification of its components, that may be potentially toxic on oral or dermal exposure, this study uses comparison between different analytical methods. The applied analytical methods were inductively coupled plasma/MS (ICP/MS), witch used to determine the metal components of the dye, high performance liquid chromatography/MS (HPLC/MS) and gas chromatography/mass spectroscopy (GC/MS) were used for qualitative and quantitative analysis of PPD in the dye. A derivatization method was applied by transforming PPD (aromatic amines) into corresponding imine derivatives. This compound was prepared by condensation of 4-methylbenzeneamine with benzaldehyed to give N-benzylidene-4-methylbenzene-amine, which is a very stable internal standard. ICP/MS analysis revealed that most metal components of hair dye are Be, Na, Al, K, Ca, Sc, Ti, V, Cr, Mn, Fe, Cu, and Zr, where HPLC/MS analysis revealed that PPD is the main ingredient of SHD. Derivatization is necessary for accurate determination of PPD in hair dye by GC/MS method and this results could not be obtained by direct injection of dye (without derivatization).
Article
Full-text available
Para-phenylenediamine is a widely used industrial chemical. Toxicity with this compound has been previously reported, but not very frequently; under-recognition of this form of poisoning in the medical community may be a cause for this. We report a case of para-phenylenediamine poisoning with the characteristic features of angioneurotic oedema, rhabdomyolysis, intravascular haemolysis, acute tubular necrosis, seizures, and death. Management is only supportive, and helpful only if instituted early; a little delay spells imminent death for the unfortunate victim. Diagnosis requires a high degree of suspicion, as the clinical features are quite distinctive.
Article
Full-text available
We studied paraphenylenediamine (PPD)-related acute kidney injury (AKI) in 81 patients and also in albino rats experimentally. In the patients' group AKI was found in 32.7%. Of them, 81.4% needed dialysis support. The overall mortality was 25.9%. In experimental rats the renal lesions were noted in all and they were glomerular congestion, intertubular (interstitial) hemorrhages, acute tubular necrosis, mesangial proliferation, and intratubular casts. The severity of renal injury appears to be dose dependent.
Article
Full-text available
1 We present a 40-year-old healthy man who developed a typical clinical picture of rhabdomyolysis following the administration of paraphenylenediamine by a witchdoctor as a pain killer. 2 Two groups of 15 mice were given paraphenylenediamine 70 mg/kg and 35 mg/kg respectively. Biochemical and histological findings of rhabdomyolysis developed in both groups, without kidney damage. 3 Paraphenylenediamine may cause rhabdomyolysis resulting in acute renal failure in humans. In mice, however, it produces rhabdomyolysis, but the kidneys are not affected.
Article
An autopsy case of rhabdomyolysis following homicidal intoxication of paraphenylenediamine was reported and the toxicological mechanism of PPD against skeletal muscles was discussed. The case was a 44 years old, previously healthy male, drinking a beverage containing PPD, prepared for a homicidal use. Total intake of PPD was about 3 g (63 mg/kg). Principal clinical manifestation of the patient was muscle rigor with tenderness, initially developed in the lower extremities and subsequently extending to all over the skeletal muscles. Laboratory examinations disclosed high CPK (137,600), LDH (3895), GOT (3400) and GPT (545), and leukocytosis (26600), indicating massive skeletal muscle necrosis. ECG revealed mild depression of ST junction in the II and aVF leads. Urine showed dark brownish discoloration and diminished in volume subsequently. Scattered necrosis of muscular fibers was observed in a biopsy of the femoral muscles. The consciousness was rather clear during the course. The patient collapsed suddenly and soon died in the course of about 30 hours. Clinically, the cause of death was thought to be acute renal failure due to rhabdomyolysis. Afterwards PPD was detected in the urine obtained in the hospital. Autopsy confirmed the clinical diagnosis: Renal collecting ductules and distal tubules were occluded by dark brownish myoglobin casts and its epithelium massively necrotized; Skeletal muscles showed scatteredly coagulation necrosis and were partially associated with inflammatory cell infiltration.
Article
Paraphenylenediamine (PPD) poisoning has been known for many years, but few studies have been devoted to the subject. We report 4 cases, seen in the nephrology department, concerning women aged from 18 to 35 years who had tried to commit suicide by drinking varying amounts of that hair dye. The initial symptom was acute asphyxia which required emergency tracheotomy in 3 cases. Thereafter, the most important visceral damage was acute renal failure, usually with oliguria or anuria, for which haemodialysis was performed in 2 cases. In these patients treated at an early stage the mid- and long-term prognosis was satisfactory. Rhabdomyolysis is the principal mechanism underlying PPD systemic toxicity; it is, in particular, responsible for the renal failure observed. The selling of PPD hair dye should be restricted by law.