Influence of 3-aminobenzamide, an inhibitor of poly(ADP-ribose)polymerase, in the evaluation of the genotoxicity of doxorubicin, cyclophosphamide and zidovudine in female mice

Sodium Butyrate Ameliorates l‐Arginine‐Induced Pancreatitis and Associated Fibrosis in Wistar Rat: Role of Inflammation and Nitrosative Stress

“…Pancreatic sections (5 μm) were taken on the poly‐ l ‐lysine‐coated slides, and after deparaffinization and rehydration slides were incubated in 0.01 M citrate buffer (pH 6.0) at 95°C for 20–30 min for antigen retrieval. Immunohistochemistry (IHC) was performed as described previously with some modifications using a commercially available kit Novolink™ polymer detection system (Leica, Milton Keynes, UK) according to manufacturer's instructions. The primary antibodies for the α‐SMA, interleukin‐1β (IL‐1β), iNOS, and 3‐nitrotyrosine were used for protein expression (Santa Cruz Biotechnology, Santa Cruz, CA).…”

Camu‐camu (Myrciaria dubia) from commercial cultivation has higher levels of bioactive compounds than native cultivation (Amazon Forest) and presents antimutagenic effects in vivo

“…Thus, regarding the colon protective effects against DMH damage, the extract compounds may act by reducing the availability of the active methyl diazonium ions generated by its metabolism in the liver, or increasing the repair activity of methylguanine methyltransferase protein (MGMT) under the formation of O6‐MeG adducts . Additionally, the camu‐camu phytochemicals could have acted against DXR mutagenicity via the following four different possibilities: (i) its activation and consequent decrease in the OH • free radicals and the lipid peroxidation produced; (ii) acting through stabilizing these free radicals generated, increasing the performance of endogenous antioxidants; (iii) decreasing the DXR inhibitory activity of the topoisomerase II enzyme; and finally (iv) preventing DNA lesions such as crosslinking, which leads to inter‐ and intra‐strand DNA damage . This results in the accumulation of DNA strand breaks, which, unless they are repaired by the cell, cause mutations in in vivo and in vitro systems.…”

PARP activation promotes nuclear AID accumulation in lymphoma cells

“…MMS is a DNA alkylating drug [ 36 ], as are other chemotherapy agents commonly used in lymphoma therapy, such as cyclophosphamide [ 37 ]. Its active metabolite alkylates N7 of guanine and generates DNA crosslinks, which are resolved by base excision repair [ 38 , 39 ]. Indeed, we found that 4-hydroperoxy-cyclophosphamide positively affects AID stabilization ( Supplementary Figure S6A ) as well as nuclear AID accumulation ( Supplementary Figure S6B and S6C ) in human Burkitt's lymphoma cells at a concentration at or above that found in cancer patients upon treatment [ 40 , 41 ].…”