Kelakai Extract Protects 

Skin From UV-Induced Oxidative

Damage
Mashuri1, Laris Donar Marukkap Sihombing2, Sabrina Alfaqihah2,
Edyson3, and Eko Suhartono3

1. Department of Radiology, Faculty of Medicine, Lambung Mangkurat University, Veteran Street No.
128, Banjarmasin 70232, South Kalimantan, Indonesia
2. Faculty of Medicine, Lambung Mangkurat University, Veteran Street No. 128, Banjarmasin 70232,
South Kalimantan, Indonesia
3. Department of Medical Chemistry/Biochemistry, Faculty of Medicine, Lambung Mangkurat
University, Ahmad Yani Street Km. 36, Banjarbaru 70712, South Kalimantan, Indonesia
Corresponding author. E-mail: esuhartono@ulm.ac.id

INTRODUCTION. Oxidative stress is a state of imbalance between oxidants and antioxidants.

Oxidative stress can be caused by ultraviolet exposure so that it can cause skin damage 1. This damage
is caused by the production of oxygen reactive compounds (ROS), for example superoxide anions,
which are excessive. Therefore, exogenous antioxidants from natural ingredients, namely kelakai, are
needed.

METHODS. This study was true experimental with research subjects in rats (Rattus norvegicus). A
total of 24 samples were grouped into 4 treatment groups. Kelakai leaves were extracted using ethanol
by maceration method. The levels of superoxide anion and superoxide dismutase enzyme activity
were measured by the Misra and Fridovich method 2.3, the carbonyl content was measured using the
modified DNPH (dinitro phenilhidrazin) method and the concentration of conjugated dienes was
measured using the Kwiat Kowska method.

RESULT AND DISCUS. Based on these results it can be concluded that kelakai extract can affect
the activity of superoxide dismutase, superoxide anion levels, carbonyl levels and conjugated dienes
of rat skin induced UV. Kelakai extract contains a compound that is capable of capturing free radicals,
namely flavonoids. The mechanism of free radical capture by flavonoids starts from the release of
electrons, forming reactive flavonoid radicals which ultimately bind to free radicals, namely
superoxide anions (Adenan, 2010). Binding of superoxide anions by reactive flavonoid radicals will
reduce the damage that occurs to proteins and lipids which in turn will reduce the levels of carbonyl
compounds and conjugated dienes.

REFERENCE
[1] D’Orazio J, Jarrett S, Amaro OA, Scott T. International Journal of Molecular Science.
14(6):12–48 (2013)
[2] Misra HP, Fridovich I. J Biol Chem. 247(10): 3170-3175 (1972)
[3] Mashuri, Ruhullah M, Putera BD, Mega VP, Putra FA, Suhartono E. Indones Biomed J.
10(2): 128-132 (2018)
 INTERACTION OF CADMIUM-SISTEIN BINDING
AND OXIDATION OF PROTEIN CAUSES OF BLOOD
TROMBOSIS
Dona Marisa1, Iwan Aflanie2, Noor Muthmainah3, Eko Suhartono4

1. Department of Physiology, Faculty of Medicine, Universitas Lambung Mangkurat, Banjarmasin

2. Department of Forensic and Medico-Legal, Faculty of Medicine, Universitas Lambung Mangkurat,
Banjarmasin
3. Department of Microbiology, Faculty of Medicine, Universitas Lambung Mangkurat, Banjarmasin
4. Department of Medical Chemistry/Biochemistry, Faculty of Medicine, Universitas Lambung
Mangkurat, Banjarmasin
Corresponding author. E-mail: esuhartono@ulm.ac.id

INTRODUCTION. Thrombosis occurs if the balance between thrombogenic factors and protective
mechanisms is disrupted. These disorders can be caused by endothelial disorders due to the presence
of heavy metals such as Cadmium (Cd). These amino acid residues can bind Cd metal covalently with
the -S-S-, -C-S-, -SH, and phenyl groups, which are present in the amino acid residues 1,2. This
situation causes changes in the structure of the protein, so that it becomes modified and forms a blood
clot (thrombosis). However, the spectroscopic interaction of cadmium-cysteine as causes of
thrombosis has not been widely studied. Therefore, this research needs to be done.

METHODS. The research conducted was an experimental study with posttest control with group
design. This study used healthy blood obtained from PMI Banjar Regency. This study used one
control group and three treatment groups, namely P0 = control group, blood without Cd; P1 = blood
group with Cd 0.003 mg/L; P2 = blood group with Cd 0.03 mg/L; P3 = blood group with Cd 0.3
mg/L; P4 = blood group with Cd 3 mg/L. Furthermore, each group was incubated for 45 minutes at
37oC. Then cloth weight, AOPP levels, and absorbance were measured at wavelengths 253 nm.

RESULT AND DISCUS. The results of the study concluded that Cd accelerated the rate of
thrombosis due to increased protein oxidation (AOPP). This oxidation is caused by binding Cd to
cysteine with Kbind = 0.355
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[1] Del Rasso NJ., Foy BD., Gearhart JM., dan Frazier. Toxicological Science, 72: 19-30
(2003)
[2] Bernhoft, RA. The Scientific World Journal.: 1-7 (2013)