Sentinel lymph node biopsy versus elective neck dissection in patients with cT1-2N0 oral tongue squamous cell carcinoma.

OBJECTIVE: This study aimed to compare the value of sentinel lymph node biopsy (SLNB) with that of elective neck dissection (END) for the prediction of cervical lymph node metastasis in patients with clinically diagnosed T1-2N0 (cT1-2N0) oral tongue squamous cell carcinoma (OTSCC), and it aimed to examine the prognostic value of individualized treatment in sentinel lymph node (SLN)-negative patients. STUDY DESIGN: The study entailed a retrospective review of 82 patients with cT1-2N0 OTSCC. Thirty patients underwent SLNB, and 52 patients underwent END. RESULTS: There was a significant difference between the SLNB and END groups in the incidence of occult cervical lymph node metastasis in initial specimens (30% vs 11.5%; P = .037). However, there were no significant differences between the groups for 10-year overall and cervical recurrence-free survival rates and 10-year overall survival rate. CONCLUSIONS: SLNB is superior to END for the prediction of cervical lymph node metastasis in patients with cT1-2N0 OTSCC. Neck dissection may be reduced for SLN-negative patients, owing to the comparable prognosis of SLNB.

Arsenite induces oxidative injury in rat brain: synergistic effect of iron.

Sodium arsenite (arsenite)-induced neurotoxicity and its interaction with ferrous citrate (iron) was investigated in rat brain. In vitro data showed that arsenite (1-10 micromol/L) concentration dependently increased lipid peroxidation and the potency of arsenite was less than that of iron. The oxidative activity of arsenite, sodium arsenate (arsenate), monomethylarsonic acid (MMA), and dimethylarsinic acid (DMA) were evaluated by inducing lipid peroxidation in cortical homogenates, and the potency for this effect was as follows: arsenite > arsenate > MMA and DMA. Several well-known antioxidants, including glutathione, melatonin, and beta-estradiol inhibited arsenite-induced lipid peroxidation in a concentration-dependent manner. Our in vivo study employed intranigral infusion of arsenite (5 nmol) in the substantia nigra (SN) of anesthetized rats. Four hours to 7 days after infusion, lipid peroxidation was elevated while glutathione was depleted in the infused SN. The dopamine content in the striatum ipsilateral to arsenite-infused SN was first elevated 24 h and then decreased 7 days after intranigral infusion of arsenite. Using pretreatment of l-buthionine-[S,R]-sulfoximine (l-BSO, i.c.v.) to reduce glutathione content in rat brain, arsenite-induced oxidative injury was augmented. Low doses of arsenite (1.5 nmol) and iron (3 nmol) alone induced minimal oxidative injury; however, co-infusion of arsenite and iron augmented neurotoxicity, including elevated lipid peroxidation and reduced striatal dopamine content. Moreover, expression of heme oxygenase-1, alpha-synuclein aggregation, and DNA fragmentation were significantly enhanced in SN co-infused with low doses of arsenite and iron. Taken together, our study demonstrates that arsenite was less potent than iron in inducing oxidative stress. Furthermore, concomitant arsenite and iron potentiated oxidative injury in the nigrostriatal dopaminergic system, indicating that interaction of metals plays a more clinically-relevant role in pathophysiology of central nervous system neurodegeneration.