Vanadium (V)-Induced Neurotoxicity in the Rat Central Nervous System: A Histo-Immunohistochemical Study

Abstract

As vanadium was found to induce oxidative stress in the central nervous system, the morphological alterations of neurons and astroglial cells in adult rat central nervous system after vanadium exposure was studied, using histological markers of cellular injury. Animals were intraperitoneally injected with 3 mg/kg body weight of sodium metavanadate for 5 consecutive days. NADPH diaphorase histochemistry and heat shock protein (hsp) 70, glial fibrillary acidic protein (GFAP), and S-100 immunohistochemistry were performed in floating sections of several brain areas. NADPHd staining was higher in the molecular and granular layers of the cerebellar cortex, and small NADPHd-stained interneurons were observed in hippocampal sections in V(+5)-exposed animals. hsp 70 immunostaining showed the presence of reactive neurons in cerebellum of treated animals. GFAP and S-100 immunohistochemistry showed enlarged astrocytes in cerebellum and hippocampus in the V(+5)-exposed animals. The histological markers used showed that the main areas affected by vanadium-mediated free-radical generation were the hippocampus and the cerebellum.

Brain Metal Distribution and Neuro-Inflammatory Profiles after Chronic Vanadium Administration and Withdrawal in Mice

“…Our study shows evidence that with chronic exposure, vanadium has a predilection for the olfactory bulb, brain stem and cerebellum. This supports the work of Haider et al (1998), Garcia et al (2005) and Ngwa et al (2014) who reported specific pathologies in the olfactory bulb, brain stem and cerebellum respectively. Further work is ongoing by us to ascertain if predilection of accumulation translates to severity of pathologies relative to other brain regions.…”

“…The number of visible astrocytes and the complexity of their processes may also be related to the extent of neural injury. Vanadium-induced astrogliosis has previously been reported in the cerebellum and hippocampus of adult rats exposed to sodium metavanadate for 5 days (Garcia et al, 2005) indicating a rapid response of astrocytes to this challenge. Astrocyte activation was also observed in the hippocampus and corpus callosum after vanadium exposure in rats of 2 weeks of age (Olopade and Connor, 2011; Todorich et al, 2011) and 3-week-old mice (Mustapha et al, 2014), indicating that reactive astrogliosis is a component of vanadium neurotoxicity.…”

“…Earlier studies have shown that vanadium crosses the blood brain barrier (García et al, 2004) to induce neuropathology including neurobehavioral (Li et al, 2013; Saxena et al, 2013; Mustapha et al, 2014; Folarin et al, 2016), neurochemical (Sasi et al, 1994; García et al, 2004) and neurocellular (Domingo, 1996; Garcia et al, 2005; Avila-Costa et al, 2006) changes. In humans, features of acute neurotoxicity include central nervous system (CNS) perturbations, (CNS) depression, tremor, impaired conditioned reflexes, as well as congestion of brain and spinal cord (Haider et al, 1998; Soazo and Garcia, 2007).…”

Anti-diabetic effects of sodium 4-amino-2,6-dipicolinatodioxovanadium(V) dihydrate in streptozotocin-induced diabetic rats

“…However, side effects, such as gastrointestinal discomfort, diarrhea, and hepatic or renal toxicity [35,36] limit their use in the treatment of diabetes. Therefore, organic vanadium compounds have been prepared with increased lipophilicity and overall absorption efficiency into the gastrointestinal tract [37].…”

Orthopaedic metals and their potential toxicity in the arthroplasty patient

“…75 Markers of oxidative damage have been identified in the brains of experimental animals exposed to Cr(VI) and V(V). 76,77 Significant alterations in visuospatial ability and attention span have been observed in male workers with a mean serum level of 14.4 ppb of V resulting from occupational exposure. 78 The heart and vascular systems.…”