Thalamic immunohistochemical assessment in Wistar rats following combined exposure to nickel and vanadium.

Abstract

BACKGROUND AND AIM: Nickel (Ni) and vanadium (V), major constituents of crude oil, have been shown to induce neurotoxic responses. However, there is paucity of reports on the impact of their combined exposure and likely potentiating consequences. This study aimed to assess the effect of Ni and V co-exposure on the thalamus of rats, by evaluating immunohistochemical markers of brain integrity including glial fibrillary acidic protein (GFAP), ionized calcium-binding adapter molecule 1 (Iba-1), neuronal nuclei antigen (NeuN), nuclear factor erythroid 2-related factor 2 (Nrf2) and parvalbumin protein.

METHODOLOGY: Twenty-four adult Wistar rats were randomly divided into four groups: saline only (Control), 20 mg/kg Ni orally for 21 days, 3 mg/kg V intraperitoneally for 7 days and combined Ni and V treatments.

RESULTS: Results showed significantly increased expression of GFAP, Iba1 and NeuN in all treatment groups. However, there was consistently marked alterations with Ni treatment compared to control with V exposures appearing to attenuate Ni impact for combined exposures. Additionally, increased Nrf2 immunoreactivity and decreased parvalbumin immunoreactivity were observed in all treatment groups compared to control.

CONCLUSION: Overall, the study demonstrates that while both Ni and V can cause toxicity in the thalamus, combined exposure showed opposing effects of their co-accumulation in the thalamus which suggests that V treatment could mitigate the Ni-induced thalamic neurotoxicity.