The impairment of motor coordination following chronic carbamazepine-levetiracetam combination treatment with evidence of corticocerebellar toxicity in male Wistar rats.

This study examined the effects of carbamazepine (CBZ) or levetiracetam (LEV) and sub-therapeutic doses of the combination of the two conventional antiepileptics on some of the markers of motor coordination. Twenty-four male Wistar rats (140 ± 5 g) were randomized into 4 groups (n = 6). Group I rats received physiological saline (0.2 ml), group II were administered CBZ (25.0 mg/kg), group III received LEV (50 mg/kg), while group IV rats were given sub-therapeutic doses of CBZ (12.5 mg/kg) and LEV (25 mg/kg) intraperitoneally for 28 days. Thereafter the animals were subjected to behavioral and biochemical investigations, while the frontal lobe and cerebellar tissue were preserved for histological investigation. Data were subjected to descriptive and inferential statistics, and the results presented as mean ± SEM, analyzed using one-way Analysis of variance (ANOVA) and Student- Newman Keuls post hoc analysis where appropriate. p < 0.05 was considered statistically significant. There was significant alteration in fine and skilled movement after the CBZ, and CBZ + LEV chronic treatment compared with the control. The CBZ, and CBZ + LEV combination treatment increased the frontal lobe and cerebellar activities of acetylcholinesterase, malondialdehyde concentration, tissue necrotic factor alpha and decreased the activities of super oxide dismutase relative to the control. Disorganization of the histoarchitecture of the frontal lobe and cerebellum was characterized by cellular atrophy, chromatolysis and hyalinization. Chronic CBZ, and CBZ + LEV combination treatment produced psychomotor dysfunction and neurotoxicity in this order CBZ + LEV > CBZ > LEV in the rats.

Cyanide-induced hyperthyroidism in male Wistar rats.

BACKGROUND: Cyanide is one of the major environmental pollutants termed thyroid disruptor. Regardless of its origin, it is a primary toxic agent. This study was designed to understand the impact of prolonged low dose cyanide exposure on the structure and function of the thyroid gland. MATERIALS AND METHODS: Twelve F1 male Wistar rats were used for this study. They were divided into two groups of six animals each. The first group served as the control group and received 0.25M sucrose while the second group being the treated group received 2 mg/kg body weight (BW) potassium hexacyanoferrate III solution. The treatment duration was 56 days following which the animals were sacrificed by cervical dislocation. Blood samples were drawn to determine serum FT3, FT4 and thyroid stimulating hormone (TSH) levels. The thyroid gland was also excised and processed for light microscopic studies. RESULT: An increase in serum FT3 and FT4 with decrease serum TSH was obtained in the treated group. Application of one-way analysis of variance (ANOVA) statistical analysis showed that there were highly significant differences (P < 0.05) in the activities of FT3, FT4 and TSH when compared with those of the control group. Light microscopic examination of thyroid gland from the treated group revealed marked epithelial hyperplasia with cellular degeneration and scanty cytoplasm while the control group revealed normal thyroid architecture. CONCLUSION: Results obtained revealed that hyperthyroidism was induced by cyanide.