Reactive Oxygen and Nitrogen Species and Their Impact on Metabolism

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are products of the regular cellular metabolism and they are well recognized for playing dual role in living systems because of their both positive and negative effects on organisms in a concentration dependent manner. For example, at low to moderate concentrations, ROS and RNS mostly play beneficial roles by their cellular responses to pathogens (Halliwell and Gutteridge 2007). On the other hand, overproduction of ROS and RNS during some pathological events, such as infections helps the organism in combating the invading pathogen induced damage. But by the same token, this overproduction may cause damage in the organism’s cell components and tissue injuries which is termed as oxidative stress (Valco et al. 2007).

Carotenoids, are yellow to red fat-soluble pigments found in plants, animals and even in microorganisms, are able to reduce the oxidative stress induced by ROS and RNS (Rodrigues et al. 2012). Potential health benefits of astaxanthine which is one of the important carotinoids reported in last few years may be partly attributed to its antioxidant and free radical scavenging properties (Dose et al. 2016). In the present study, the aim was to evaluate if astaxanthin can improve the behavior of depressed mice. In this context, reserpine was used to induce depression. Mice exposed to reserpine demonstrated decreased locomotion and exploration activity reduced social interaction decreased mobility time in FST and TST which confirmed the construct validity of the disease model.

There is evidence that inhibition of monoamine re-uptake or depletion of monoamines in the brain can cause depression-like symptoms in animals (Gao et al 2016). Moreover, acute reserpine treatment has been found to cause rapid reduction hypothalamic and pituitary catecholamines level (Tang 1991). Open field test (OFT) is considered as one of the most widely used measures of behavioral test in animal psychology (Walsh et al 1976) though it was initially developed as a test to measure emotionality in rodents (Hall 1934). In OFT, the rearing behavior, an exploratory act displayed by mice when placed in a novel situation, is considered as an indicator of anxiety (Carli et al 1989).

Treatment of astaxanthin reduces free radical damage, apoptosis, and cerebral infarction in ischemia-related injury in the brain of adult rats (Shen et al 2009). Astaxanthin supplemented algal powder was found to have memory improving effects in lower doses in BALB/c mice (Zhang et al 2007). Anxiogenic compounds significantly reduced the number of entries into and percentage of time spent on the open arms; on the other hand, anxiolytic compounds significantly increased these parameters in elevated plus maze test (Pellow et al 1985).

Previous reports have shown that oxidative stress is associated with depression, anxiety, and related psychiatric disorders. Treatment of mice with reserpine, an inducer of oxidative stress, causes anxiety-like behavior through the NADPH oxidase pathway [12]. In fact, a phosphodiesterase-2 inhibitor reversed the oxidative stress-induced anxiety through an increase in cyclic guanosine monophosphate signaling [12]. Thus, phosphodiesterase-2 may be a novel pharmacological target for treatment of anxiety in neuropsychiatric and neurodegenerative disorders that involve oxidative stress. Another report has also suggested a linear and significant relationship between the intracellular redox status of peripheral blood granulocytes and the different parameters of anxiety-related behavior [13].

The present study showed that the duration of immobility was increased in FST and TST when the mice, exposed to reserpine. Similar result was seen in previous studies. Since the result of the present study was similar to the previous studies, it can be concluded that depression was successfully induced. In our present study, we found using astaxanthin has increased the time spent in the open arm in elevated plus maze. Similar observation was seen in [16] But this increase in time spent in open arm was not that significant in our study. In a previous study astaxanthin was administered for 15 days where as in our study it was administered for 7 days. And in this 7 days improvement, although not significant, was observed. Therefore, according to the previous study if astaxanthin was administered for 15 days maybe more improvements would have been observed.

The immobility time, in case of FST and TST, of reserpine induced depressed mice, when exposed to astaxanthin have shown to improve in our study. Comparable result was obtained in [16]. But this decrease in immobility was not of much significance. Similar results were seen in a previous study [16] where different milligrams of astaxanthin were administered per kg body weight of mice. In that study it was seen that the different doses of astaxanthin did not show much change in immobility of FST ans TST. Similarly, in our study the decrease in immobility of astaxanthine exposed depressed mice in FST and TST was not that significant. Therefore, as we got similar results, we can conclude as was mentioned in the previous study [16] that astaxanthin shows anxiolytic effect more prominently than anti-depressant.