Involvement of oxidative stress and pro-inflammatory cytokines in copper sulfate-induced depression-like disorders and abnormal neuronal morphology in mice.

Epidemiological studies have implicated copper as one of the key environmental risk factors for the pathogenesis of depression. However, the precise mechanism by which copper contribute to the genesis of depression particularly the involvement of oxidative stress-driven neuroinflammation is yet to be fully investigated. Thus, this study was designed to evaluate the effects of copper sulfate (CuSO) on depression-like behaviors and the role of oxidative stress and pro-inflammatory cytokines in mice.

D-ribose-L-cysteine reduces oxidative stress and inflammatory cytokines to mitigate liver damage, and memory decline induced by copper sulfate in mice.

Background: Current evidences have implicated copper in amyloid aggregation that trigger the downstream oxidative stress-mediated neuroinflammation that characterized memory deterioration in patients with Alzheimer's disease (AD). Thus, this study was designed to evaluate the effect of D-Ribose-L-Cysteine (DRLC), a potent antioxidant agent, on copper sulfate (CuSO)-induced memory deterioration and the biochemical mechanisms underpinning its action in mice.

Methods: Male Swiss mice were randomly distributed into 5 groups (n = 10/group).