@entity871 exposure in @entity19 leads to @entity1283 and voltage-gated @entity972 (Kv) channel remodeling. Because redox balance of @entity10402 affects Kv function and @entity871 alters cellular redox potential, we hypothesized that @entity871 exposure leads to cardiac @entity132 and redox changes resulting in @entity943 . In the present study, we investigated the electrical changes and redox abnormalities caused by 72h @entity871 treatment in @entity19 . Cardiac repolarization changes were assessed by acquiring electrocardiogram (ECG) and cardiac action potentials (AP). Biochemical assays were employed to identify the @entity10402 changes, @entity68473 expression and @entity296 . @entity871 treatment caused marked @entity1168 , @entity943 and significantly prolonged (ms) the, RR (186.2  10.7 vs. 146.4  6.2), PR (46.8  3.1 vs. 39.3  1.6), QRS (10.8  0.6 vs. 8.5  0.2), QTc (57.1  3.5 vs. 40  1.4) and JT (13.4  2.1 vs. 7.0  0.5) intervals, when compared with normoxia group. @entity871 treatment also induced significant increase in cardiac action potential duration (APD) (ex-APD90; 73.8  9.5 vs. 50.9  3.1ms) and elevated levels of serum markers of @entity296 ; cardiac troponin I (TnI) and @entity880 dehydrogenase (LDH). @entity871 exposure altered cardiac levels of mRNA/protein expression of; @entity68473 , Kvb subunits and @entity14075 , and increased ratios of reduced @entity10402 ( @entity2125 / @entity2125 _ @entity1110 / @entity1110 ). Inhibition of @entity14075 in H9C2 cells using @entity68474 resulted in decreased @entity14075 and @entity68473 expression, suggesting that @entity14075 may mediate @entity68473 downregulation. In conclusion, the @entity1370 effects of @entity871 exposure involve @entity132 and redox changes resulting in @entity943 .

High level of oxygen treatment causes @entity1370 with XXXX and redox modulation.

@entity2125 :: ('MESH:D009243', 'Chemical') :: ['NADH', 'NAD'] @entity296 :: ('MESH:D009202', 'Disease') :: ['myocardial injury'] @entity132 :: ('MESH:D010468', 'Disease') :: ['ion channel disturbances'] @entity68473 :: ('16493(Tax:10090)', 'Gene') :: ['Kv1.5'] @entity871 :: ('MESH:D018496', 'Disease') :: ['Hyperoxia', 'hyperoxia'] @entity1283 :: ('MESH:D006332', 'Disease') :: ['cardiac hypertrophy'] @entity19 :: ('10090', 'Species') :: ['mice'] @entity1168 :: ('MESH:D001919', 'Disease') :: ['bradycardia'] @entity1110 :: ('MESH:D009249', 'Chemical') :: ['NADP', 'NADPH'] @entity1370 :: ('MESH:D066126', 'Disease') :: ['cardiotoxic'] @entity68474 :: ('MESH:C444426', 'Chemical') :: ['Splitomicin'] @entity880 :: ('MESH:D019344', 'Chemical') :: ['lactate'] @entity972 :: ('MESH:D011188', 'Chemical') :: ['potassium'] @entity14075 :: ('93759(Tax:10090)', 'Gene') :: ['SiRT1'] @entity943 :: ('MESH:D001145', 'Disease') :: ['arrhythmias', 'arrhythmia'] @entity10402 :: ('CHEBI:36980', 'Chemical') :: ['pyridine nucleotides', 'pyridine nucleotide']
@entity943 :: (MESH:D001145,Disease) :: ['arrhythmias']
