Antioxidant

Antioksidan adalah senyawa yang mampu menangkal atau meredam dampak negatif
oksidan dalam tubuh. Antioksidan bekerja dengan cara mendonorkan satu elektronnya
kepada senyawa yang bersifat oksidan sehingga aktivitas senyawa oksidan tersebut dapat
dihambat. Antioksidan dikelompokkan menjadi 2 yaitu antioksidan enzim (endogen) dan
non-enzim. Antioksidan enzim misalnya enzim superoksida dismutase (SOD), katalase (CAT),
dan glutation peroksidase (GPx), Antioksidan non-enzim (eksogen) banyak ditemukan dalam
sayuran dan buah-buahan, yang meliputi glutation tereduksi (GSH), vitamin C, E, β-karoten,
flavonoid, isoflavon, flavon, antosianin, katekin, dan isokatekin, serta asam lipoat.
Rendahnya antioksidan enzim dapat digunakan sebagai petanda tingginya kadar radikal
bebas dalam tubuh. Review berikut bertujuan untuk memberikan gambaran tentang peran
antioksidan dalam mencegah terbentuknya radikal bebas dalam tubuh (Siti Thomas, 2017).

ROS diproduksi sebagai zat antara, dan tingkat sel mereka sangat diatur oleh berbagai enzim
detoksifikasi, seperti SOD, glutathione peroxidase (GPX), dan katalase (CAT), atau oleh berbagai
antioksidan, termasuk flavonoid, asam askorbat, vitamin E, dan glutathione (GSH). Ada korelasi yang
signifikan antara generasi ROS dan metabolisme, serta dengan patofisiologi seluler
Ketidakseimbangan reduksi-oksidasi (redoks) merupakan peran penting dalam
keseimbangan antara generasi ROS dan netralisasi kelebihan ROS oleh faktor antioksidan seluler.
Homeostasis redoks yang terganggu menyebabkan efek berbahaya pada sel yang dimediasi oleh
gangguan pada mekanisme pensinyalan sel atau mengakibatkan kerusakan oksidatif pada
biomolekul, seperti protein, lipid, dan asam nukleat (Ahmed Adhal, 2017).
Diagram enzim antioxidant dalam menghadapi ROS.

Perlindungan antioxidant dalam sel

Study penelitian mengatakan bahwa terapi HBO dapat meningkatkan antioxidant

diantaranya yaitu Glutayhion (GSH), Super peroxida dismutase (SOD), Copper (Cu), Zinc (Zn)
(Hadi Suyono, 2018). Contoh mekanisme SOD,catalase, dan GPx dalam mengeliminasi ROS
(Siti Thomas, 2017).
 Sumber radikal bebas

Sumber ROS
stress oksidative karena genetik
Polymorphic variants related to the metabolism of methionine transmethylation and
transsulfuration, which increase susceptibility to endogenous and environmental oxidative stress,
are significantly different in children with autism. 91–93 Studies show a decreased ability in children
with these genetic variants to handle oxidative stress as measured by several metabolic biomarkers
including S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), adenosine, homocysteine,
cystathionine, cysteine, oxidized and reduced glutathione, endogenous secretory receptor for
advanced glycation end-products (RAGE), and the pro-inflammatory ligand S100A9. In addition,
polymorphisms in glutathione pathways, which modulate the response to oxidative stress, strongly
affect risk for autism. For example, the homozygous GSTM1 deletion genotype imposes a near 2-fold
increased risk for autism.94,95 Further, polymorphisms of the glutathione S-transferase P1 gene
(GSTP1) in the mother, which could affect the fetus during pregnancy, are high risk factors for the
induction of autism (OR = 2.67, CI 95% = 1.39–5.13). 96 Thus, several genetic variants that affect
pathways involved in oxidative stress are risk factors for autism (william Parker,2017)
stress oksidatif karena lingkungan

Exposure to environmental toxins, a source of oxidative stress, has been

associated with autism in a number of studies.49 Maternal exposure during
gestation to agricultural pesticides such as organophosphates,
organochlorines, and pyrethroids has been identified as a moderate-to-high
risk factor for autism.50–52 The risk seems to be dependent at least in part on the
proximity to the applied chemical and the trimester during which the exposure
took place. However, the data are somewhat noisy and, as pointed out by the
authors, possibly confounded by unavoidable misclassifications in the
estimations of maternal exposure. In contrast to evidence of the effects of
exposure in utero, evidence for exposure to pesticides after birth as a risk
factor for autism is slim to non-existent. Maternal exposure to traffic-related
air pollutants also carries risk factors for autism. For example, exposure to
particulate matter during the third trimester is a low-to-moderate risk factor
for autism,53–55 while maternal exposure to other traffic-related toxins (e.g.
mercury, lead, arsenic, cadmium, manganese, styrene, trichloroethylene, and
vinyl chloride) is a moderate-to-high risk factor for autism (Wiliam Parker,
2017)
increased oxidative stress is a primary risk factor for the pathophysiology of
many neuropsychiatric disorders such as the Parkinson disease, the Alzheimer
disease, the Huntington disease, and multiple sclerosis. 16,17 Numerous oxidative
stress markers (antioxidant enzymes, lipid peroxidation, and protein/DNA
oxidation) were detected in abnormal levels in autistic children, such as protein
dityrosine.18,19 Several studies have documented reduced levels of glutathione,
glutathione peroxidase, methionine, and cysteine besides elevated levels of
oxidized glutathione in children with autism.12,20 The excreted antioxidants are
lower in autistic patients compared with healthy age-matching subjects and
upon correlation with severity of the disease, such as superoxide
dismutase.21,22 Also, ceruloplasmin and transferrin antioxidants show
suboptimal levels in serum of autistic children, leading to abnormal
metabolism of toxic and oxidative stress–mediating metal ions.23 Recent
genetic studies have identified variants of some antioxidant enzyme-coding
genes that increase the susceptibility to autism. For example, the interaction
between glutathione S-transferase P1 and glutathione S-transferase M1
mutated genes contributed to autism risk (Nagwa A Meguid,2017).
Several studies have measured inflammation and oxidative stress changes
before and after HBOT in children with autism. Rossignol et al  evaluated 18
15

children 3 to 16 years of age with autism who underwent 45 minutes each of

HBOT at either 1.5 ATA and 100% oxygen or at 1.3 ATA and 24% oxygen for a
total of 40 sessions. Markers of oxidative stress, including plasma oxidized
glutathione before and after treatment, did not change significantly in either
group. Both groups demonstrated improvement trends in mean C-reactive
protein (CRP) levels, especially children who had higher CRP levels at the onset
of treatment. When results for all 18 children were pooled, a significant
improvement in CRP levels was found (P = .021). Clinical outcome ratings by
parents before and after treatment also showed statistically significant
improvement. Bent et al  studied cytokine level changes before and after 80
16

sessions of HBOT in 10 children aged 3 to 8. All children reportedly

experienced improvements based on several parent-completed measures of
behaviour. However, these children did not have abnormal cytokine levels at
baseline, and no statistically significant changes were noted in any of the 29
measured cytokines over the course of the study ( Teeranai Sakulchi, 2017)