ABSTRACT
Aim: This study was aimed at understanding the earlier findings involving chronic, lowlevel cyanide exposure resulting from eating poorly processed cassava products associated with the development of goitre as seen in cassava endemic regions of Nigeria. Study Design: 30F1 female adult Wistar rats were divided into five (5) groups of 6 animals each. Groups 1 to 4 represented the treatment groups while group 5 was the control of the experiment. The cyanide treatment dose were; group1: 20mg/KgBW, group 2: 12mg/KgBW, group 3: 6mg/KgBW and group 4: 2mg/KgBW while the control group received 0.25M Sucrose. Place and Duration of Study: The animal facility of College of Health Sciences, Osun State University, Osogbo, Osun State, Nigeria. The treatment duration was 30days. Methodology: Animals were sacrificed by cervical dislocation. The blood samples were collected to determine Serum FT3, FT4 and TSH concentration. The thyroid gland was excised and processed for light microscopic examination; while the activities of G6PDH, LDH, ALP, MDA and SOD were assayed from the thyroid tissue homogenates. Results: Histological observation of thyroid gland of rats from the experimental treated groups revealed markedly distended follicles and diffusely hyperplastic thyroid follicles lined with tall columnar epithelial cells. These thyroid epithelial cells are crowded and enlarged projecting into the lumens of their respective follicles. Their interstitial tissue all had dilated blood vessels. Application of one-way ANOVA statistical analytical method showed that there were highly significant differences P˂0.05 in the activities of G6PDH, LDH, ALP, MDA, SOD, FT3, FT4 and TSH when compared with those of the control group. Conclusion: The results obtained from this study showed hyperthyroidism was effectively induced by cyanide.
ABSTRACT
Background: The cerebellum, also called the little brain is an organ concerned with regulation of movement and other associated motor functions. It is believed to be phylogenetically one of the oldest parts of the brain. It accounts for one tenth of the brain volume and contains approximately 50% of the total brain neuron. Damage to the cerebellum is major factor involved in the progression of movement disorders. Aim: To investigate possibility of selective neuronal vulnerability in neurotoxicity and the etiology of neurodegenerative diseases especially those involving movement disorders originating from the cerebellum. Method: F1 Generation adult Wistar rats were treated with 20 and 10 mg/Kg BW of potassium cyanide (KCN), the cerebellar cortex was harvested and processed for immunohistochemistry of cell cycle markers (anti-p53 and anti-Bax) and the neuronal glycolytic pathway marker; Neuron Specific Enolase (anti-NSE). Antigen retrieval method was used specifically as peroxidase anti peroxidase reaction (PAP). The reaction was developed using a polymer 3’3’Diaminobenzidine tetrachloride (DAB), intensified in Methenamine Silver and counterstained in Hematoxylin. Results: Cyanide toxicity induced apoptosis in the cerebellum via a pathway involving Bax in mitochondria dysregulation (mitochondria apoptotic signaling) and a cytoplasmic pathway involving p53 (a nucleolase). The NSE expression level also indicates associated metabolic dysregulation with alteration in expression of cell cycle proteins. Conclusion: Cyanide toxicity induced cell death in the cerebellar cortex by metabolic alteration (NSE) and ROS formation. The expression of Bax and p53 showed that apoptosis was triggered via a mitochondria/Bax dependent, p53 related apoptotic pathway.
ABSTRACT
Aims: This study aims at investigating possible means of reducing cyanide toxicity by blocking NMDA R1 via ketamine (an NMDA R1 antagonist). This is to provide a template for quick arrest of cyanide toxicity in neurons under oxygen deprived condition. Place and Duration of Study: Bingham University, Department of Anatomy, Karu, Nigeria. The duration of the study was100 minutes. Methodology: Freshly harvested cortical tissue blocks were perfused in accessory cerebrospinal fluid (ACSF) containing all the necessary salts and glucose. The cultures were treated with ACSF (Control), ACSF+KCN (potassium cyanide), ACSF+KCN+Ketamine and ACSF+Ketamine for a total duration of 100 minutes at 37ºC. Results: The Ketamine had a protective and reversal effects on the tissues both for oxygen deprivation and cyanide toxicity, The cells in tissues treated with ACSF+KCN+Ketamine showed normal appearance of cell body and axonal projections, the cells treated with ACSF+Ketamine showed fewer degenerating cells compared to those treated with cyanide. Conclusion: Ketamine, an NMDA R1 antagonist is neuroprotective against the toxicity of cyanide.