[ABSTRAK
Kerusakan oksidatif DNA yang disebabkan oleh propil galat (PG) dan 2,6-di-tertbutil-p-benzoquinon (BHT-Quinon, metabolit BHT), dianalisis dari pembentukanDNA adduct, 8-hidroksi-􀀕􀂶-deoksiguanosin (8-OHdG), terhadap Calf thymus􀀧􀀱􀀤􀀃􀁇􀁄􀁑􀀃􀁅􀁄􀁖􀁄􀀃􀁗􀁘􀁑􀁊􀁊􀁄􀁏􀀃􀀧􀀱􀀤􀀏􀀃􀀕􀂶-deoksiguanosin (dG) secara in vitro. PG dengandimediasi oleh CuCl2 menyebabkan peningkatan 8-OHdG terhasap Calf thymusDNA sebesar 9,17 kali lebih besar dibandingkan terhadap kontrol (DNA tanpaperlakuan). Dengan adanya CuCl2 pada konsentrasi 1,28.10-5 M, rasiopembentukan 8-OHdG dari hasil interaksi antara dG dengan PG pada berbagaivariasi konsentrasi (20 􀂱 150 ppm) berkisar antara 75,50 􀂱 312,06 8-OHdGterhadap 105 dG. Pembentukan 8-OHdG tersebut, meningkat denganbertambahnya konsentrasi PG dari 20 􀂱 80 ppm, kemudian mulai menurun denganbertambahnya konsentrasi PG. BHT-quinon, dengan adanya CuCl2 menyebabkanpeningkatan 8-OHdG terhadap Calf thymus DNA sebesar 0,05 kali dibandingkankontrol (DNA tanpa perlakuan). Analisis menggunakan LC-MS/MS dilakukanuntuk mengidentifikasi 8-OHdG, dengan puncak induk (M+. + 1) 284 danmemiliki dua fragmen utama m/z 167,9 dan m/z 139,9.

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ABSTRACT>/b>

Oxidative DNA damage caused by propyl gallate (PG) and 2,6-di-tert-butyl-pbenzoquinone

(BHT-Quinone, a metabolite of butylated hydroxytoluene 􀂱 BHT),

was evaluated by measuring the formation of DNA adduct, 8-hydroxy-􀀕􀂶-

deoxyguanosine (8-OHdG), in Calf thymus DNA and DNA base, 􀀕􀂶-

deoxyguanosine (dG). PG mediated with CuCl2 increased 8-OHdG formation in

Calf thymus DNA 9.17 fold from control (DNA without treatment). In the present

of CuCl2 1.28.10-5 M, ratio 8-OHdG resulted from interaction of dG with PG at

various concentration (20 􀂱 150 ppm), was ranged from 75.50 􀂱 312.06 8-OHdG

per 105 dG. This formation was increased by PG in a concentration-dependent

manner ranged from 20 ppm up to 80 ppm, then decreased upon increasing the PG

concentration. Meanwhile, BHT-quinone increased 0.05 fold from control (DNA

without treatment) in the presence of CuCl2. LC-MS/MS analysis was performed

to identify molecular structure of 8-OHdG, which had base peak (M+. + 1) 284 and

had two main fragment at m/z 167.9 and m/z 139.9., Oxidative DNA damage caused by propyl gallate (PG) and 2,6-di-tert-butyl-pbenzoquinone

(BHT-Quinone, a metabolite of butylated hydroxytoluene 􀂱 BHT),

was evaluated by measuring the formation of DNA adduct, 8-hydroxy-􀀕􀂶-

deoxyguanosine (8-OHdG), in Calf thymus DNA and DNA base, 􀀕􀂶-

deoxyguanosine (dG). PG mediated with CuCl2 increased 8-OHdG formation in

Calf thymus DNA 9.17 fold from control (DNA without treatment). In the present

of CuCl2 1.28.10-5 M, ratio 8-OHdG resulted from interaction of dG with PG at

various concentration (20 􀂱 150 ppm), was ranged from 75.50 􀂱 312.06 8-OHdG

per 105 dG. This formation was increased by PG in a concentration-dependent

manner ranged from 20 ppm up to 80 ppm, then decreased upon increasing the PG

concentration. Meanwhile, BHT-quinone increased 0.05 fold from control (DNA

without treatment) in the presence of CuCl2. LC-MS/MS analysis was performed

to identify molecular structure of 8-OHdG, which had base peak (M+. + 1) 284 and

had two main fragment at m/z 167.9 and m/z 139.9.]