Theoretically speaking – No, we generally expect decrease in lipid peroxidation with increase in antioxidant status of any system/cell.  However, it is equally important to know that expression of genes of antioxidant enzymes such as SOD, CAT and GSH increase on exposure of living systems to stress. It is likely that medicinal plant extract/material might be inducing some kind of stress, which could be promoting expression of genes or might be having certain molecules, which could be promoting expression of genes of antioxidant enzymes. Simultaneously, certain molecules of the medicinal plant could be promoting lipid peroxidation.

Can you please precisely let me know how you are using medicinal plant material (are you using powder or extract or something else – if extract is it aqueous, alcoholic or non-aqueous extract)? When we are using plant material, we are not 100% sure regarding what all molecules present in the extract would be responsible for the effect we are measuring. Therefore, I believe that one should use purified active component of the medicinal plant material to precisely address one’s query.

see the link 

Antioxidant activity, lipid peroxidation and skin diseases. What's new.

Briganti S, Picardo M.

J Eur Acad Dermatol Venereol. 2003 Nov;17(6):663-9. Review.

PMID:

14761133

Theoretically speaking – No, we generally expect decrease in lipid peroxidation with increase in antioxidant status of any system/cell.  However, it is equally important to know that expression of genes of antioxidant enzymes such as SOD, CAT and GSH increase on exposure of living systems to stress. It is likely that medicinal plant extract/material might be inducing some kind of stress, which could be promoting expression of genes or might be having certain molecules, which could be promoting expression of genes of antioxidant enzymes. Simultaneously, certain molecules of the medicinal plant could be promoting lipid peroxidation.

Can you please precisely let me know how you are using medicinal plant material (are you using powder or extract or something else – if extract is it aqueous, alcoholic or non-aqueous extract)? When we are using plant material, we are not 100% sure regarding what all molecules present in the extract would be responsible for the effect we are measuring. Therefore, I believe that one should use purified active component of the medicinal plant material to precisely address one’s query.

What tecnique are you using to measure lipid peroxidation? If you are using TBARS, many factors causes false positives such as presence of carbohydrates or aldehydes in the medium. If you extract contain carbohydrate- or aldehyde-like molecules, that might be a reason.

Another probable reason is that the antioxidant capability of your extract is such that is disrupting ROS signalling modulating physiological processes like autophagy. Excessive removing of ROS may also be deleterious for cell for that reason.

Many plant antioxidants also display prooxidant activity dependently on dose used and other conditions (media composition, etc). As prooxidants, they are able induce antioxidant defense and in the same time lead to oxidative damages.

I experienced the similar results with Hypericum extracts. However none of the isolated compounds from hypericum extract was prooxidant.

Go to the following link. Sometimes it happens that along with the antioxident levels, lipid peroxidation level also increases. It actually depends on the components found in the plant and the pathway they follow under invivo condition.

http://www.ncbi.nlm.nih.gov/pubmed/11127401

I agree with p.Pardha- Saradhi generally speaking there is a good correlation between total phenolic contents of a plant extracts and their ability to inhibit lipid per oxidation  also certain type of compounds may depleted  intracellular thrills including reduced glutathione lead to imbalance in GSH redox status.This could lead to increase in lipid per oxidation this depend also in type of extraction used plant parts.check the saponins contents good luck

I have experience with food and some natural antioxidants could be pro-oxidant, depend of their concentration.

Dear Ifeoluwa

The answer for your question can be found in this article: 

Lipid peroxidation and irreversible cell damage: synergism between carbon tetrachloride and 1,2-dibromoethane in isolated rat hepatocytes.

Danni O1, Chiarpotto E, Aragno M, Biasi F, Comoglio A, Belliardo F, Dianzani MU, Poli G.

Toxicol Appl Pharmacol. 1991 Sep 1;110(2):216-22.

Abstract

The combination of 1,2-dibromoethane (DBE) with carbon tetrachloride (CCl4) in the isolated rat hepatocyte model produces a significant potentiation of both lipid peroxidation and plasma membrane damage induced by the latter compound. The increase in malondialdehyde production precedes the hepatocyte damage, evaluated in terms both of lactate dehydrogenase leakage and trypan blue exclusion. When hepatocytes are isolated from vitamin E pretreated rats, both the prooxidant and the cytotoxic effects of CCl4 are prevented. Also the synergism between CCl4 and DBE on lipid peroxidation disappears completely while that on cell damage is strongly reduced. The increased lipid peroxidation appears to be one of the mechanisms of the observed synergism between CCl4 and DBE on hepatocyte damage. Regarding the antioxidant status of the hepatocyte challenged with CCl4 and DBE, an early and significant consumption of vitamin E is observed only in the presence of the mixture of these xenobiotics. Total nonprotein thiol content is not significantly modified by CCl4 poisoning while DBE, alone and in association with CCl4, markedly decreases it. Vitamin E supplementation does not prevent but moderately delays total nonprotein thiol depletion due to DBE or to the mixture. Finally, glutathione transferase activity is significantly reduced by CCl4 treatment and not by DBE, and vitamin E supplementation totally prevents such inhibition. The increased prooxidant effect of CCl4 plus DBE compared to CCl4 alone seems related to the shift in DBE metabolism consequent to the CCl4-dependent inactivation of glutathione transferase.

Probably the carbon tetrachloride induced liver injury via free radicals generation.It is well proved that oxidative stress constitutes an important risk factor for tissue/cell damage. The changes included also cell membranes labilisation (fluidity of cells’ membranes). Malondialdehyde (MDA), a toxic aldehydic end product of lipid peroxidation is belived to be largely responsible for the cytopathologic effects observed during the oxidative stress of lipid peroxidation. The oxidation/antioxidation disturbances are linked in ‘cause-result’ relation with cellular membranes labilization.

definitely depends on solvent system during the extract

Lets get it clear: you are talking of lipid PEROXIDATION  and not oxidation in general. Therefore, peroxidation might increase at the cost of mere oxidation of FAs.

Definitely, it happen. As plant consist of variety of chemical having multi targeting effect.

Why not - both are different phenomenon - and you are using crude extracts I suppose

Yes, I am working with crude extract

Dear Ifeoluwa T Oyeyemi

I am attaching literature on the anticancer properties. I hope they will be useful to you.

I recommend the fruit of Rhus coriaria L. (Anacardiaceae) for your research.

Good luck.